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Medicine LibreTexts

18.2: Structure and Function of Blood Vessels

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  • Page ID 22383

  • Whitney Menefee, Julie Jenks, Chiara Mazzasette, & Kim-Leiloni Nguyen
  • Reedley College, Butte College, Pasadena City College, & Mt. San Antonio College via ASCCC Open Educational Resources Initiative

By the end of this section, you will be able to:

  • Compare and contrast the three tunics that make up the walls of most blood vessels
  • Distinguish between elastic arteries, muscular arteries, and arterioles on the basis of structure, location, and function
  • Compare and contrast the three types of capillaries on the basis of structure, location, and function
  • Describe the basic structure of a capillary bed, from the supplying metarteriole to the venule into which it drains
  • Compare and contrast veins, venules, and venous sinuses on the basis of structure, location, and function
  • Discuss several factors affecting blood flow in the venous system

Blood is carried through the body via blood vessels. An artery is a blood vessel that carries blood away from the heart, where it branches into ever-smaller vessels. Eventually, the smallest arteries, vessels called arterioles, further branch into tiny capillaries, where nutrients and wastes are exchanged, and then combine with other vessels that exit capillaries to form venules, small blood vessels that carry blood to a vein, a larger blood vessel that returns blood to the heart.

Blood flow is the movement of blood through a vessel, tissue, or organ. The slowing or blocking of blood flow is called resistance. Blood pressure is the force that blood exerts upon the walls of the blood vessels or chambers of the heart. The components of blood pressure include systolic pressure, which results from ventricular contraction, and diastolic pressure, which results from ventricular relaxation. Pulse, the expansion and recoiling of an artery, reflects the heartbeat. In the arterial system, vasodilation and vasoconstriction of the arterioles is a significant factor in systemic blood pressure: slight vasodilation greatly decreases resistance and increases flow, whereas slight vasoconstriction greatly increases resistance and decreases flow. In the arterial system, as resistance increases, blood pressure increases and flow decreases. In the venous system, constriction increases blood pressure as it does in arteries; the increasing pressure helps to return blood to the heart. In addition, constriction causes the vessel lumen to become more rounded, decreasing resistance and increasing blood flow.

Arteries and veins transport blood in two distinct circuits: the systemic circuit and the pulmonary circuit (Figure \(\PageIndex{1}\)). The systemic circuit begins in the left atrium of the heart and ends in the venae cavae and coronary sinus that drain into the right atrium. Systemic arteries provide blood rich in oxygen to the body’s tissues; this blood is often referred to as oxygenated blood. The blood returned to the heart through systemic veins has less oxygen, since much of the oxygen carried by the arteries has been delivered to the cells; this blood is often referred to as deoxygenated blood. In contrast, the pulmonary circuit begins in the right atrium and ends in the pulmonary veins that drain into the left atrium. Pulmonary arteries carry blood low in oxygen exclusively to the lungs for gas exchange. Pulmonary veins then return freshly oxygenated blood from the lungs to the heart to be pumped back out into systemic circulation. Although arteries and veins differ structurally and functionally, they share certain features.

Pulmonary and systemic circuits of blood flow with artery, capillary bed, and vein for each. Systemic circuit includes four examples supplying upper body, kidney, lower body, and the two capillary beds of the hepatic portal system.

Structural Characteristics of Vessels

Different types of blood vessels vary slightly in their structures, but they share the same general features. Arteries and arterioles have thicker walls than veins and venules because they are closer to the heart and receive blood that is surging at a far greater pressure (Figure \(\PageIndex{2}\)). Each type of vessel has a lumen —a hollow passageway through which blood flows. Arteries have smaller lumens than veins, a characteristic that helps to maintain the pressure of blood moving through the system. Together, their thicker walls and smaller diameters give arterial lumens a more rounded appearance in cross section than the lumens of veins.

Structure and proportions of the three vessel tunics and lumen of arteries and veins are compared via diagram and micrograph.

By the time blood has passed through capillaries and entered venules, the pressure initially exerted upon it by heart contractions has diminished. In other words, in comparison to arteries, venules and veins withstand a much lower pressure from the blood that flows through them. Their walls are considerably thinner and their lumens are correspondingly larger in diameter, allowing more blood to flow with less vessel resistance. In addition, many veins of the body, particularly those of the limbs, contain valves that assist the unidirectional flow of blood toward the heart. This is critical because blood flow becomes sluggish in the extremities, as a result of the lower pressure and the effects of gravity.

The walls of arteries and veins are largely composed of living cells and their products (including collagen and elastic fibers); the cells require nourishment and produce waste. Since blood passes through the larger vessels relatively quickly, there is limited opportunity for blood in the lumen of the vessel to provide nourishment to or remove waste from the vessel’s cells. Further, the walls of the larger vessels are too thick for nutrients to diffuse through to all of the cells. Larger arteries and veins contain small blood vessels within their walls known as the vasa vasorum —literally “vessels of the vessel”—to provide them with this critical exchange. Since the pressure within arteries is relatively high, the vasa vasorum must function in the outer layers of the vessel (see Figure \(\PageIndex{2}\)) or the pressure exerted by the blood passing through the vessel would collapse it, preventing any exchange from occurring. The lower pressure within veins allows the vasa vasorum to be located closer to the lumen. The restriction of the vasa vasorum to the outer layers of arteries is thought to be one reason that arterial diseases are more common than venous diseases, since their location makes it more difficult to nourish the cells of the arteries and remove waste products. There are also minute nerves within the walls of both types of vessels that control the contraction and dilation of smooth muscle. These minute nerves are known as the nervi vasorum .

Both arteries and veins have the same three distinct tissue layers, called tunics (from the Latin term tunica, for the garments first worn by ancient Romans). From the most interior layer to the outer, these tunics are the tunica intima, the tunica media, and the tunica externa (see Figure \(\PageIndex{2}\)). Table \(\PageIndex{1}\) compares and contrasts the tunics of the arteries and veins.

Tunica Intima

The tunica intima (also called the tunica interna) is composed of epithelial and connective tissue layers. Lining the tunica intima is the specialized simple squamous epithelium called the endothelium, which is continuous throughout the entire vascular system, including the lining of the chambers of the heart. Damage to this endothelial lining and exposure of blood to the collagen fibers beneath is one of the primary causes of clot formation. Until recently, the endothelium was viewed simply as the boundary between the blood in the lumen and the walls of the vessels. Recent studies, however, have shown that it is physiologically critical to such activities as helping to regulate capillary exchange and altering blood flow. The endothelium releases local chemicals called endothelins that can constrict the smooth muscle within the walls of the vessel to increase blood pressure. Uncompensated overproduction of endothelins may contribute to hypertension (high blood pressure) and cardiovascular disease.

Next to the endothelium is the basement membrane, or basal lamina, that effectively binds the endothelium to the connective tissue. The basement membrane provides strength while maintaining flexibility, and it is permeable, allowing materials to pass through it. The thin outer layer of the tunica intima contains a small amount of areolar connective tissue that consists primarily of elastic fibers to provide the vessel with additional flexibility; it also contains some collagen fibers to provide additional strength.

In larger arteries, there is also a thick, distinct layer of elastic connective tissue known as the internal elastic membrane (also called the internal elastic lamina) at the boundary with the tunica media. Like the other components of the tunica intima, the internal elastic membrane provides structure while allowing the vessel to stretch. It is permeated with small openings that allow exchange of materials between the tunics. The internal elastic membrane is not apparent in veins. In addition, many veins, particularly in the lower limbs, contain one-way valves formed by sections of thickened endothelium that are reinforced with connective tissue, extending into the lumen.

Under the microscope, the lumen and the entire tunica intima of a vein will appear smooth, whereas those of an artery will normally appear wavy because of the partial constriction of the smooth muscle in the tunica media, the next layer of blood vessel walls.

Tunica Media

The tunica media is the substantial middle layer of the vessel wall (see Figure \(\PageIndex{2}\)). It is generally the thickest layer in arteries, and it is much thicker in arteries than it is in veins. The tunica media consists of layers of smooth muscle supported by connective tissue that is primarily made up of elastic fibers, most of which are arranged in circular sheets. Toward the outer portion of the tunic, there are also layers of longitudinal smooth muscle. Contraction and relaxation of the circular muscles decrease and increase the diameter of the vessel lumen, respectively. Specifically in arteries, vasoconstriction decreases blood flow as the smooth muscle in the walls of the tunica media contracts, making the lumen narrower and increasing blood pressure. Similarly, vasodilation increases blood flow as the smooth muscle relaxes, allowing the lumen to widen and blood pressure to drop. Both vasoconstriction and vasodilation are regulated in part by small vascular nerves, known as nervi vasorum , or “nerves of the vessel,” that run within the walls of blood vessels. Neural and chemical mechanisms reduce or increase blood flow in response to changing body conditions, from exercise to hydration.

The smooth muscle layers of the tunica media are supported by a framework of collagen fibers that also binds the tunica media to the inner and outer tunics. Along with the collagen fibers are large numbers of elastic fibers that appear as wavy lines in prepared slides. Separating the tunica media from the outer tunica externa in larger arteries is the external elastic membrane (also called the external elastic lamina), which also appears wavy in slides. This structure is not usually seen in smaller arteries, nor is it seen in veins.

Tunica Externa

The outer tunic, the tunica externa (also called the tunica adventitia), is a substantial sheath of dense irregular connective tissue composed primarily of collagen fibers. Some bands of elastic fibers are found here as well. The tunica externa in veins also contains groups of smooth muscle fibers. This is normally the thickest tunic in veins and may be thicker than the tunica media in some larger arteries. The outer layers of the tunica externa are not distinct but rather blend with the surrounding connective tissue outside the vessel, helping to hold the vessel in relative position. If you are able to palpate some of the superficial veins on your upper limbs and try to move them, you will find that the tunica externa prevents this. If the tunica externa did not hold the vessel in place, any movement would likely result in disruption of blood flow.

An artery is a blood vessel that conducts blood away from the heart. All arteries have relatively thick walls that can withstand the high pressure of blood ejected from the heart. However, those close to the heart have the thickest walls, containing a high percentage of elastic fibers in all three of their tunics. This type of artery is known as an elastic artery (Figure \(\PageIndex{3}\)). Vessels larger than 10 mm in diameter are typically elastic. Their abundant elastic fibers allow them to expand, as blood pumped from the ventricles passes through them, and then to recoil after the surge has passed. If artery walls were rigid and unable to expand and recoil, their resistance to blood flow would greatly increase and blood pressure would rise to even higher levels, which would in turn require the heart to pump harder to increase the volume of blood expelled by each pump and maintain adequate pressure and flow. Artery walls would have to become even thicker in response to this increased pressure. The elastic recoil of the vascular wall helps to maintain the pressure gradient that drives the blood through the arterial system. An elastic artery is also known as a conducting artery, because the large diameter of the lumen gives it a low resistance and enables it to accept a large volume of blood from the heart which is conducted to smaller branches within regions of the body.

Comparison of vessel tunics in different types of arteries

Farther from the heart, where the surge of blood has dampened, the percentage of elastic fibers in an artery’s tunica intima decreases and the amount of smooth muscle in its tunica media increases. The artery at this point is described as a muscular artery . The diameter of muscular arteries typically ranges from 0.1 mm to 10 mm. Their thick tunica media allows muscular arteries to play a leading role in vasoconstriction which controls blood flow to individual organs. In contrast, their decreased quantity of elastic fibers limits their ability to expand. Fortunately, because the blood pressure has eased by the time it reaches these more distant vessels, elasticity has become less important.

Notice that although the distinctions between elastic and muscular arteries are important, there is no “line of demarcation” where an elastic artery suddenly becomes muscular. Rather, there is a gradual transition as the vascular tree repeatedly branches. In turn, muscular arteries branch to distribute blood to the vast network of arterioles that deliver blood to capillaries within specific organs and tissues. For this reason, a muscular artery is also known as a distributing artery.

An arteriole is a very small artery that leads to a capillary. Arterioles have the same three tunics as the larger vessels, but the thickness of each is greatly diminished. The critical endothelial lining of the tunica intima is intact. The tunica media is restricted to one or two smooth muscle cell layers in thickness. The tunica externa remains but is very thin as arterioles are supported and held in place by their positioning within organs and tissues (see Figure \(\PageIndex{3}\)).

With a lumen averaging 30 micrometers or less in diameter, arterioles are critical in slowing down—or resisting—blood flow and, thus, causing a substantial drop in blood pressure. Because of this, you may see them referred to as resistance vessels. The muscle fibers in arterioles are normally slightly contracted, causing arterioles to maintain a consistent muscle tone—in this case referred to as vascular tone—in a similar manner to the muscular tone of skeletal muscle. In reality, all blood vessels exhibit vascular tone due to the partial contraction of smooth muscle. The importance of the arterioles is that they will be the primary site of both resistance and regulation of blood pressure. The precise diameter of the lumen of an arteriole at any given moment is determined by neural and chemical controls, and vasoconstriction and vasodilation in the arterioles are the primary mechanisms for distribution of blood flow to capillary beds as well as regulation of systemic blood pressure.

DISORDERS OF THE...

Cardiovascular System: Arteriosclerosis

Compliance allows an artery to expand when blood is pumped through it from the heart, and then to recoil after the surge has passed. This helps promote blood flow. In arteriosclerosis, compliance is reduced, and pressure and resistance within the vessel increase. This is a leading cause of hypertension and coronary heart disease, as it causes the heart to work harder to generate a pressure great enough to overcome the resistance.

Arteriosclerosis begins with injury to the endothelium of an artery, which may be caused by irritation from high blood glucose, infection, tobacco use, excessive blood lipids, and other factors. Artery walls that are constantly stressed by blood flowing at high pressure are also more likely to be injured—which means that hypertension can promote arteriosclerosis, as well as result from it.

Recall that tissue injury causes inflammation. As inflammation spreads into the artery wall, it weakens and scars it, leaving it stiff (sclerotic). As a result, compliance is reduced. Moreover, circulating triglycerides and cholesterol can seep between the damaged lining cells and become trapped within the artery wall, where they are frequently joined by leukocytes, calcium, and cellular debris. Eventually, this buildup, called plaque, can narrow arteries enough to impair blood flow. The term for this condition, atherosclerosis (athero- = “porridge”) describes the mealy deposits (Figure \(\PageIndex{4}\)).

Atherosclerosis involves calcified, fatty plaques that build up in a damaged artery wall and narrow the diameter of the artery, causing ischemia.

Sometimes a plaque can rupture, causing microscopic tears in the artery wall that allow blood to leak into the tissue on the other side. When this happens, platelets rush to the site to clot the blood. This clot can further obstruct the artery and—if it occurs in a coronary or cerebral artery—cause a sudden heart attack or stroke. Alternatively, plaque can break off and travel through the bloodstream as an embolus until it blocks a more distant, smaller artery.

Even without total blockage, vessel narrowing leads to ischemia—reduced blood flow—to the tissue region “downstream” of the narrowed vessel. Ischemia in turn leads to hypoxia—decreased supply of oxygen to the tissues. Hypoxia involving cardiac muscle or brain tissue can lead to cell death and severe impairment of brain or heart function.

A major risk factor for both arteriosclerosis and atherosclerosis is advanced age, as the conditions tend to progress over time. Arteriosclerosis is normally defined as the more generalized loss of compliance, “hardening of the arteries,” whereas atherosclerosis is a more specific term for the build-up of plaque in the walls of the vessel and is a specific type of arteriosclerosis. There is also a distinct genetic component, and pre-existing hypertension and/or diabetes also greatly increase the risk. However, obesity, poor nutrition, lack of physical activity, and tobacco use all are major risk factors.

Treatment includes lifestyle changes, such as weight loss, smoking cessation, regular exercise, and adoption of a diet low in sodium and saturated fats. Medications to reduce cholesterol and blood pressure may be prescribed. For blocked coronary arteries, surgery is warranted. In angioplasty, a catheter is inserted into the vessel at the point of narrowing, and a second catheter with a balloon-like tip is inflated to widen the opening. To prevent subsequent collapse of the vessel, a small mesh tube called a stent is often inserted. In an endarterectomy, plaque is surgically removed from the walls of a vessel. This operation is typically performed on the carotid arteries of the neck, which are a prime source of oxygenated blood for the brain. In a coronary bypass procedure, a non-vital superficial vessel from another part of the body (often the great saphenous vein) or a synthetic vessel is inserted to create a path around the blocked area of a coronary artery.

Capillaries

A capillary is a microscopic channel that supplies blood to the tissues, through a process called perfusion . Exchange of gases and other substances occurs in the capillaries between the blood and the surrounding cells and their tissue fluid (interstitial fluid). The diameter of a capillary lumen ranges from 5–10 micrometers; the smallest are just barely wide enough for an erythrocyte to squeeze through. Flow through capillaries is often described as microcirculation .

The wall of a capillary consists of the endothelial layer surrounded by a basement membrane with occasional smooth muscle fibers. Some variation in wall structure is seen depending on the size of the capillary. In a large capillary, several endothelial cells bordering each other may line the lumen, while in a small capillary, there may be only a single cell layer that wraps around to contact itself.

For capillaries to function, their walls must be leaky, or permeable , allowing some substances to pass through. There are three major types of capillaries, which differ according to their degree of permeability: continuous, fenestrated, and sinusoid capillaries (Figure \(\PageIndex{5}\)).

Continuous Capillaries

The most common type of capillary, the continuous capillary , is found in almost all vascularized tissues. Continuous capillaries are characterized by a complete endothelial lining with tight junctions between endothelial cells. Although a tight junction is usually impermeable and only allows for the passage of water and ions, they are often incomplete in capillaries, leaving intercellular clefts that allow for exchange of water and other very small molecules between the blood plasma and the interstitial fluid. Substances that can pass between cells include metabolic products, such as glucose, water, and small hydrophobic molecules like gases and hormones, as well as various leukocytes. Continuous capillaries not associated with the brain are rich in transport vesicles, contributing to either endocytosis or exocytosis. Those in the brain are part of the blood-brain barrier. Here, there are tight junctions and no intercellular clefts, plus a thick basement membrane and astrocyte extensions called end feet; these structures combine to prevent the movement of nearly all substances.

Comparison of anatomy of different types of capillaries

Fenestrated Capillaries

A fenestrated capillary is one that has pores (or fenestrations) in addition to tight junctions in the endothelial lining. These make the capillary permeable to larger molecules. The number of fenestrations and their degree of permeability vary according to their location. Fenestrated capillaries are common in the small intestine, which is the primary site of nutrient absorption, as well as in the kidneys, which filter the blood. They are also found in the choroid plexus of the brain and many endocrine structures, including the hypothalamus, pituitary, pineal, and thyroid glands.

Sinusoid Capillaries

A sinusoid capillary (or sinusoid) is the least common type of capillary and the most permeable. Sinusoid capillaries are flattened, and they have extensive intercellular gaps and incomplete basement membranes, in addition to intercellular clefts and fenestrations. This gives them an appearance similar to Swiss cheese. These very large openings allow for the passage of the largest molecules, including plasma proteins and even cells. Blood flow through sinusoids is very slow, allowing more time for exchange of gases, nutrients, and wastes. Sinusoids are found in the liver and spleen, bone marrow, lymph nodes (where they carry lymph, not blood), and many endocrine glands including the pituitary and adrenal glands. Without these specialized capillaries, these organs would not be able to provide their myriad functions. For example, when bone marrow forms new blood cells, the cells must enter the blood supply and can only do so through the large openings of a sinusoid capillary; they cannot pass through the small openings of continuous or fenestrated capillaries. The liver also requires extensive specialized sinusoid capillaries in order to process the materials brought to it by the hepatic portal vein from both the digestive tract and spleen, and to release plasma proteins into circulation.

Metarterioles and Capillary Beds

A metarteriole is a type of vessel that has structural characteristics of both an arteriole and a capillary. Slightly larger than the typical capillary, the smooth muscle of the tunica media of the metarteriole is not continuous but forms rings of smooth muscle (sphincters) prior to the entrance of the capillaries. Each metarteriole arises from a terminal arteriole and branches to supply blood to a capillary bed that may consist of 10–100 capillaries depending on the metabolic needs of the surrounding tissues.

The precapillary sphincters , circular smooth muscle cells that surround the capillary at its origin with the metarteriole, tightly regulate the flow of blood from a metarteriole to the capillaries it supplies. Their function is critical: If all of the capillary beds in the body were to open simultaneously, they would collectively hold every drop of blood in the body and there would be none in the arteries, arterioles, venules, veins, or the heart itself. Normally, the precapillary sphincters are closed. When the surrounding tissues need oxygen and have excess waste products, the precapillary sphincters open, allowing blood to flow through and exchange to occur before closing once more (Figure \(\PageIndex{6}\)). If all of the precapillary sphincters in a capillary bed are closed, blood will flow from the metarteriole directly into a thoroughfare channel and then into the venous circulation, bypassing the capillary bed entirely. This creates what is known as a vascular shunt . In addition, some regions contain one or more arteriovenous anastomoses , which can be opened to bypass the capillary bed, skipping perfusion and leading directly to the venous system.

Although you might expect blood flow through a capillary bed to be smooth, in reality, it moves with an irregular, pulsating flow. This pattern is called vasomotion and is regulated by chemical signals that are triggered in response to changes in internal conditions, such as oxygen, carbon dioxide, hydrogen ion, and lactic acid levels. For example, during strenuous exercise when oxygen levels decrease and carbon dioxide, hydrogen ion, and lactic acid levels all increase, the capillary beds in skeletal muscle are open, as they would be in the digestive system when nutrients are present in the digestive tract. During sleep or rest periods, vessels in both areas are largely closed; they open only occasionally to allow oxygen and nutrient supplies to travel to the tissues to maintain basic life processes.

Anatomy of a Capillary Bed

A venule is an extremely small vein, generally 8–100 micrometers in diameter. Postcapillary venules drain multiple capillaries exiting from a capillary bed. Multiple venules join to form veins. The walls of venules consist of endothelium, a thin or non-existent middle layer with a few smooth muscle cells and elastic fibers, plus an outer layer of connective tissue fibers that constitute a very thin tunica externa (Figure \(\PageIndex{7}\)). Venules as well as capillaries are the primary sites of emigration or diapedesis, in which the white blood cells adhere to the endothelial lining of the vessels and then squeeze between adjacent cells to enter the tissue fluid.

A vein is a blood vessel that conducts blood toward the heart. Compared to arteries, veins are thin-walled vessels with large and irregular lumens (see Figure \(\PageIndex{2}\)). Because they are low-pressure vessels, larger veins are commonly equipped with valves that promote the unidirectional flow of blood toward the heart and prevent backflow toward the capillaries caused by the inherent low blood pressure in veins as well as the pull of gravity (Figure \(\PageIndex{7}\)).

Comparison of Types of Veins

Venous System

The pumping action of the heart propels the blood into the arteries, from an area of higher pressure toward an area of lower pressure. If blood is to flow from the veins back into the heart, the pressure in the veins must be greater than the pressure in the atria of the heart. Two factors help maintain this pressure gradient between the veins and the heart. First, the pressure in the atria during diastole is very low, often approaching zero when the atria are relaxed (atrial diastole). Second, two physiologic “pumps” increase pressure in the venous system. The use of the term “pump” implies a physical device that speeds flow. These physiological pumps are less obvious.

Skeletal Muscle Pump

In many body regions, the pressure within the veins can be increased by the contraction of the surrounding skeletal muscle. This mechanism, known as the skeletal muscle pump (Figure \(\PageIndex{8}\)), helps the lower-pressure veins counteract the force of gravity, increasing pressure to move blood back to the heart. As leg muscles contract, for example during walking or running, they exert pressure on nearby veins with their numerous one-way valves. This increased pressure causes blood to flow upward, opening valves superior to the contracting muscles so blood flows through. Simultaneously, valves inferior to the contracting muscles close; thus, blood should not seep back downward toward the feet. Military recruits are trained to flex their legs slightly while standing at attention for prolonged periods. Failure to do so may allow blood to pool in the lower limbs rather than returning to the heart. Consequently, the brain will not receive enough oxygenated blood, and the individual may lose consciousness.

2114_Skeletal_Muscle_Vein_Pump.jpg

Respiratory Pump

The respiratory pump aids blood flow through the veins of the thorax and abdomen. During inhalation, the volume of the thorax increases, largely through the contraction of the diaphragm, which moves downward and compresses the abdominal cavity. The elevation of the chest caused by the contraction of the external intercostal muscles also contributes to the increased volume of the thorax. The volume increase causes air pressure within the thorax to decrease, allowing us to inhale. Additionally, as air pressure within the thorax drops, blood pressure in the thoracic veins also decreases, falling below the pressure in the abdominal veins. This causes blood to flow along its pressure gradient from veins outside the thorax, where pressure is higher, into the thoracic region, where pressure is now lower. This in turn promotes the return of blood from the thoracic veins to the atria. During exhalation, when air pressure increases within the thoracic cavity, pressure in the thoracic veins increases, speeding blood flow into the heart while valves in the veins prevent blood from flowing backward from the thoracic and abdominal veins.

Cardiovascular System: Edema and Varicose Veins

Despite the presence of valves and the contributions of other anatomical and physiological adaptations we will cover shortly, over the course of a day, some blood will inevitably pool, especially in the lower limbs, due to the pull of gravity. Any blood that accumulates in a vein will increase the pressure within it, which can then be reflected back into the smaller veins, venules, and eventually even the capillaries. Increased pressure will promote the flow of fluids out of the capillaries and into the interstitial fluid. The presence of excess tissue fluid around the cells leads to a condition called edema.

Most people experience a daily accumulation of tissue fluid, especially if they spend much of their work life on their feet (like most health professionals). However, clinical edema goes beyond normal swelling and requires medical treatment. Edema has many potential causes, including hypertension and heart failure, severe protein deficiency, renal failure, and many others. In order to treat edema, which is a sign rather than a discrete disorder, the underlying cause must be diagnosed and alleviated.

Photograph of left leg with varicose veins visible as lumps under the skin.

Edema may be accompanied by varicose veins, especially in the superficial veins of the legs ( Figure \(\PageIndex{9}\) ). This disorder arises when defective valves allow blood to accumulate within the veins, causing them to distend, twist, and become visible on the surface of the integument. Varicose veins may occur in both sexes, but are more common in women and are often related to pregnancy. More than simple cosmetic blemishes, varicose veins are often painful and sometimes itchy or throbbing. Without treatment, they tend to grow worse over time. The use of support hose, as well as elevating the feet and legs whenever possible, may be helpful in alleviating this condition. Laser surgery and interventional radiologic procedures can reduce the size and severity of varicose veins. Severe cases may require conventional surgery to remove the damaged vessels. As there are typically redundant circulation patterns, that is, anastomoses, for the smaller and more superficial veins, removal does not typically impair the circulation. There is evidence that patients with varicose veins suffer a greater risk of developing a thrombus or clot.

Veins as Blood Reservoirs

In addition to their primary function of returning blood to the heart, veins may be considered blood reservoirs, since systemic veins contain approximately 64 percent of the blood volume at any given time (Figure \(\PageIndex{10}\), Table \(\PageIndex{3}\)). Their ability to hold this much blood is due to their high capacitance , that is, their capacity to distend (expand) readily to store a high volume of blood, even at a low pressure. The large lumens and relatively thin walls of veins make them far more distensible than arteries; thus, they are said to be capacitance vessels .

Chart to visualize the distribution of blood flow that is presented in table format elsewhere.

Concept Review

Blood pumped by the heart flows through a series of vessels known as arteries, arterioles, capillaries, venules, and veins before returning to the heart. Arteries transport blood away from the heart and branch into smaller vessels, forming arterioles. Arterioles distribute blood to capillary beds, the sites of exchange with the body tissues. Capillaries lead back to small vessels known as venules that flow into the larger veins and eventually back to the heart.

Arteries, arterioles, venules, and veins are composed of three tunics known as the tunica intima, tunica media, and tunica externa. The tunica intima is a thin layer composed of a simple squamous epithelium known as endothelium and a small amount of connective tissue. The tunica media is a thicker area composed of variable amounts of smooth muscle and connective tissue. It is the thickest layer in all but the largest arteries. The tunica externa is primarily a layer of connective tissue, although in veins, it also contains some smooth muscle. Blood flow through vessels can be dramatically increased or decreased by vasoconstriction and vasodilation. The arterial system is a relatively high-pressure system, so arteries have thick walls that appear round in cross section. The venous system is a lower-pressure system, containing veins that have larger lumens and thinner walls. They often appear flattened. Capillaries have only a tunica intima layer.

Review Questions

Q. The endothelium is found in the ________.

A. tunica intima

B. tunica media

C. tunica externa

Q. Nervi vasorum control ________.

A. vasoconstriction

B. vasodilation

C. capillary permeability

D. both vasoconstriction and vasodilation

Q. Closer to the heart, arteries would be expected to have a higher percentage of ________.

A. endothelium

B. smooth muscle fibers

C. elastic fibers

D. collagen fibers

Q. Which of the following best describes veins?

A. thick walled, small lumens, low pressure, lack valves

B. thin walled, large lumens, low pressure, have valves

C. thin walled, small lumens, high pressure, have valves

D. thick walled, large lumens, high pressure, lack valves

Q. An especially permeable type of capillary found in the liver and certain other tissues is called a ________.

A. capillary bed

B. fenestrated capillary

C. sinusoid capillary

D. metarteriole

Critical Thinking Questions

Q. Arterioles are often referred to as resistance vessels. Why?

A: Arterioles receive blood from arteries, which are vessels with a much larger lumen. As their own lumen averages just 30 micrometers or less, arterioles are critical in slowing down—or resisting—blood flow. The arterioles can also constrict or dilate, which varies their resistance, to help distribute blood flow to the tissues.

Q. A blood vessel with a few smooth muscle fibers and connective tissue, and only a very thin tunica externa conducts blood toward the heart. What type of vessel is this?

A: This is a venule.

Q. An obese patient comes to the clinic complaining of swollen feet and ankles, fatigue, shortness of breath, and often feeling “spaced out.” She is a cashier in a grocery store, a job that requires her to stand all day. Outside of work, she engages in no physical activity. She confesses that, because of her weight, she finds even walking uncomfortable. Explain how the skeletal muscle pump might play a role in this patient’s signs and symptoms.

A. People who stand upright all day and are inactive overall have very little skeletal muscle activity in the legs. Pooling of blood in the legs and feet is common. Venous return to the heart is reduced, a condition that in turn reduces cardiac output and therefore oxygenation of tissues throughout the body. This could at least partially account for the patient’s fatigue and shortness of breath, as well as her “spaced out” feeling, which commonly reflects reduced oxygen to the brain.

Contributors and Attributions

OpenStax Anatomy & Physiology (CC BY 4.0). Access for free at  https://openstax.org/books/anatomy-and-physiology

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Biology LibreTexts

18.12: Laboratory Activities and Assignment

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  • Page ID 53799

  • Rosanna Hartline
  • West Hills College Lemoore

Laboratory Activities and Assignment

Part 1: review of blood vessels.

1. On the diagram of a blood vessel below, label the following:

Tissues of Blood vessel diagram for labeling

2. For each description below, write one of the choices below in the blank spaces provided. Choices can be used more than once.

  • capillaries

a. __________________ These large blood vessels carry blood to the heart.

b. __________________ & __________________ These blood vessels contain valves.

c. __________________ These large blood vessels carry blood away from the heart.

d. __________________ These smaller blood vessels carry blood from the vessels of where materials are transferred between the blood and the tissues to the large blood vessels carrying blood to the heart.

e. __________________ These are the smallest blood vessels in the body.

f. __________________ These smaller blood vessels carry blood to the vessels where materials are transferred between the blood and the tissues.

g. __________________ The inferior vena cava is one of these.

h. __________________ The aorta is one of these.

i. __________________ The vessels where materials are transferred between the blood and the tissues.

j. __________________, __________________, & __________________ Blood vessels that do not have valves.

3. Name the arteries on the diagram below. Use the choices given to fill in each blank.

Artery diagram for labeling

3. Label the following arteries on the diagram below:

4. Label the following arteries on the diagram below:

Artery diagram for labeling

5. Label the following arteries on the diagram below:

Artery diagram for labeling

6. Write the number in each blank that corresponds with the name of each artery in the diagram.

7. Label the following veins on the diagrams below:

Vein diagram for labeling

6. Label the following veins on the diagrams below:

Vein diagram for labeling

Part 2: Examining the Histology of the Blood Vessels

  • Obtain the slides listed below that are available for today’s lab.
  • Focus on each sample and identify the structures listed for each type of tissue.
  • Indicate the total magnification you make each illustration at in the space provided.
  • Illustrate each tissue you observe with the microscope at the magnification you listed.
  • Label each illustration with the structures listed for each.

Large Elastic Artery Cross Section

Label the tissue with: tunica interma, tunica media, tunica adventitia, smooth muscle, elastic fibers, vasa vasorum

Capillary-Containing Tissue

Label the tissue with: capillary, nucleus of endothelial cell

Vein Cross Section

Label the tissue with: tunica interma, tunica media, tunica adventitia, nucleus of endothelial cell, valve

Part 3: The Arteries and Veins of the Systemic Circuit

  • For each blood vessel in the table below, identify it on anatomical models, anatomical diagrams provided by your instructor, or on the virtual model at www.zygotebody.com .
  • Fill out the table to tell the location of the blood vessel.
  • Indicate whether this blood vessel supplies blood or drains it by checking the appropriate box.
  • Tell what organs or body regions are supplied or drained by the blood vessel.
  • Indicate whether this blood vessel is paired (right and left) or if there is only one by checking the appropriate box.

Blood Vessels of the Trunk

Blood vessels of the head and neck, blood vessels of the upper limbs, blood vessels of the lower limbs, attributions.

  • "Anatomy and Physiology Lab Homework" by Laird C Sheldahl is licensed under CC BY-SA 4.0
  • "Aorta branches.svg" by Mikael Häggström is licensed under CC BY-SA 3.0 / A derivative from the original work
  • "Digital Histology" by Department of Anatomy and Neurobiology and the Office of Faculty Affairs , Virginia Commonwealth University School of Medicine and the ALT Lab at Virginia Commonwealth University is licensed under CC BY 4.0
  • "Gray's Anatomy plates" by Henry Vandyke Carte is in the Public Domain
  • "Medical gallery of Blausen Medical 2014" by Blausen.com staff is licensed under CC BY 3.0
  • "Thigh arteries schema numbered.svg" by Jecowa is licensed under CC BY 3.0 / A derivative from the original work
  • "BIOL 250 Human Anatomy Lab Manual SU 19" by Yancy Aquino , Skyline College is licensed under CC BY-NC-SA 4.0
  • "Systemic Blood Vessels" by Dongho Kim is licensed under CC BY-NC-SA 4.0

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18.5 Hemostasis

Learning objectives.

By the end of this section, you will be able to:

Describe the process of hemostasis

  • Describe the three mechanisms involved in hemostasis
  • Explain how the extrinsic and intrinsic coagulation pathways lead to the common pathway, and the coagulation factors involved in each
  • Discuss disorders affecting hemostasis

Platelets are key players in hemostasis , the process by which the body seals a ruptured blood vessel and prevents further loss of blood. Although rupture of larger vessels usually requires medical intervention, hemostasis is quite effective in dealing with small, simple wounds. There are three steps to the process: vascular spasm, the formation of a platelet plug, and coagulation (blood clotting). Failure of any of these steps will result in hemorrhage —excessive bleeding.

Vascular Spasm

When a vessel is severed or punctured, or when the wall of a vessel is damaged, vascular spasm occurs. In vascular spasm , the smooth muscle in the walls of the vessel contracts dramatically. This smooth muscle has both circular layers; larger vessels also have longitudinal layers. The circular layers tend to constrict the flow of blood, whereas the longitudinal layers, when present, draw the vessel back into the surrounding tissue, often making it more difficult for a surgeon to locate, clamp, and tie off a severed vessel. The vascular spasm response is believed to be triggered by several chemicals called endothelins that are released by vessel-lining cells and by pain receptors in response to vessel injury. This phenomenon typically lasts for up to 30 minutes, although it can last for hours.

Formation of the Platelet Plug

In the second step, platelets, which normally float free in the plasma, encounter the area of vessel rupture with the exposed underlying connective tissue and collagenous fibers. The platelets begin to clump together, become spiked and sticky, and bind to the exposed collagen and endothelial lining. This process is assisted by a glycoprotein in the blood plasma called von Willebrand factor, which helps stabilize the growing platelet plug . As platelets collect, they simultaneously release chemicals from their granules into the plasma that further contribute to hemostasis. Among the substances released by the platelets are:

  • adenosine diphosphate (ADP), which helps additional platelets to adhere to the injury site, reinforcing and expanding the platelet plug
  • serotonin, which maintains vasoconstriction
  • prostaglandins and phospholipids, which also maintain vasoconstriction and help to activate further clotting chemicals, as discussed next

A platelet plug can temporarily seal a small opening in a blood vessel. Plug formation, in essence, buys the body time while more sophisticated and durable repairs are being made.

Coagulation

More sophisticated and durable repairs made beyond the plug formation are collectively called coagulation , the formation of a blood clot. The process is sometimes characterized as a cascade, because one event prompts the next as in a multi-level waterfall. The result is the production of a gelatinous but robust clot made up of a mesh of fibrin —an insoluble filamentous protein derived from fibrinogen, the plasma protein introduced earlier—in which platelets and blood cells are trapped. Figure 18.5.1 summarizes the three steps of hemostasis following injury.

This figure details the steps in the clotting of blood. Each step is shown along with a detailed text box describing the steps on the left. On the right, a signaling pathway shows the different chemical signals involved in the clotting process.

Clotting Factors Involved in Coagulation

In the coagulation cascade, chemicals called clotting factors (or coagulation factors) prompt reactions that activate still more coagulation factors. The process is complex, but is initiated along two basic pathways:

  • The extrinsic pathway, which normally is triggered by trauma.
  • The intrinsic pathway, which begins in the bloodstream and is triggered by internal damage to the wall of the vessel.

Both of these merge into a third pathway, referred to as the common pathway (see Figure 18.5.1 b ). All three pathways are dependent upon the 12 known clotting factors, including Ca 2+ and vitamin K ( Table 18.1 ). Clotting factors are secreted primarily by the liver and the platelets. The liver requires the fat-soluble vitamin K to produce many of them. Vitamin K (along with biotin and folate) is somewhat unusual among vitamins in that it is not only consumed in the diet but is also synthesized by bacteria residing in the large intestine. The calcium ion, considered factor IV, is derived from the diet and from the breakdown of bone. Some recent evidence indicates that activation of various clotting factors occurs on specific receptor sites on the surfaces of platelets.

The 12 clotting factors are numbered I through XIII according to the order of their discovery. Factor VI was once believed to be a distinct clotting factor, but is now thought to be identical to factor V. Rather than renumber the other factors, factor VI was allowed to remain as a placeholder and also a reminder that knowledge changes over time.

Extrinsic Pathway

The quicker responding and more direct extrinsic pathway (also known as the tissue factor pathway) begins when damage occurs to the surrounding tissues, such as in a traumatic injury. Upon contact with blood plasma, the damaged extravascular cells, which are extrinsic to the bloodstream, release factor III (thromboplastin). Sequentially, Ca 2+ then factor VII (proconvertin), which is activated by factor III, are added, forming an enzyme complex. This enzyme complex leads to activation of factor X (Stuart–Prower factor), which activates the common pathway discussed below. The events in the extrinsic pathway are completed in a matter of seconds.

Intrinsic Pathway

The intrinsic pathway (also known as the contact activation pathway) is longer and more complex. In this case, the factors involved are intrinsic to (present within) the bloodstream. The pathway can be prompted by damage to the tissues, resulting from internal factors such as arterial disease; however, it is most often initiated when factor XII (Hageman factor) comes into contact with foreign materials, such as when a blood sample is put into a glass test tube. Within the body, factor XII is typically activated when it encounters negatively charged molecules, such as inorganic polymers and phosphate produced earlier in the series of intrinsic pathway reactions. Factor XII sets off a series of reactions that in turn activates factor XI (antihemolytic factor C or plasma thromboplastin antecedent) then factor IX (antihemolytic factor B or plasma thromboplasmin). In the meantime, chemicals released by the platelets increase the rate of these activation reactions. Finally, factor VIII (antihemolytic factor A) from the platelets and endothelial cells combines with factor IX (antihemolytic factor B or plasma thromboplasmin) to form an enzyme complex that activates factor X (Stuart–Prower factor or thrombokinase), leading to the common pathway. The events in the intrinsic pathway are completed in a few minutes.

Common Pathway

Both the intrinsic and extrinsic pathways lead to the common pathway , in which fibrin is produced to seal off the vessel. Once factor X has been activated by either the intrinsic or extrinsic pathway, the enzyme prothrombinase converts factor II, the inactive enzyme prothrombin, into the active enzyme thrombin . (Note that if the enzyme thrombin were not normally in an inactive form, clots would form spontaneously, a condition not consistent with life.) Then, thrombin converts factor I, the insoluble fibrinogen, into the soluble fibrin protein strands. Factor XIII then stabilizes the fibrin clot.

Fibrinolysis

The stabilized clot is acted upon by contractile proteins within the platelets. As these proteins contract, they pull on the fibrin threads, bringing the edges of the clot more tightly together, somewhat as we do when tightening loose shoelaces (see Figure 18.5.1 a ). This process also wrings out of the clot a small amount of fluid called serum , which is blood plasma without its clotting factors.

To restore normal blood flow as the vessel heals, the clot must eventually be removed. Fibrinolysis is the gradual degradation of the clot. Again, there is a fairly complicated series of reactions that involves factor XII and protein-catabolizing enzymes. During this process, the inactive protein plasminogen is converted into the active plasmin , which gradually breaks down the fibrin of the clot. Additionally, bradykinin, a vasodilator, is released, reversing the effects of the serotonin and prostaglandins from the platelets. This allows the smooth muscle in the walls of the vessels to relax and helps to restore the circulation.

Plasma Anticoagulants

An anticoagulant is any substance that opposes coagulation. Several circulating plasma anticoagulants play a role in limiting the coagulation process to the region of injury and restoring a normal, clot-free condition of blood. For instance, a cluster of proteins collectively referred to as the protein C system inactivates clotting factors involved in the intrinsic pathway. TFPI (tissue factor pathway inhibitor) inhibits the conversion of the inactive factor VII to the active form in the extrinsic pathway. Antithrombin inactivates factor X and opposes the conversion of prothrombin (factor II) to thrombin in the common pathway. And as noted earlier, basophils release heparin , a short-acting anticoagulant that also opposes prothrombin. Heparin is also found on the surfaces of cells lining the blood vessels. A pharmaceutical form of heparin is often administered therapeutically, for example, in surgical patients at risk for blood clots.

External Website

QR Code representing a URL

View these animations to explore the intrinsic, extrinsic, and common pathways that are involved the process of coagulation. The coagulation cascade restores hemostasis by activating coagulation factors in the presence of an injury. How does the endothelium of the blood vessel walls prevent the blood from coagulating as it flows through the blood vessels?

Disorders of Clotting

Either an insufficient or an excessive production of platelets can lead to severe disease or death. As discussed earlier, an insufficient number of platelets, called thrombocytopenia, typically results in the inability of blood to form clots. This can lead to excessive bleeding, even from minor wounds.

Another reason for failure of the blood to clot is the inadequate production of functional amounts of one or more clotting factors. This is the case in the genetic disorder hemophilia , which is actually a group of related disorders, the most common of which is hemophilia A, accounting for approximately 80 percent of cases. This disorder results in the inability to synthesize sufficient quantities of factor VIII. Hemophilia B is the second most common form, accounting for approximately 20 percent of cases. In this case, there is a deficiency of factor IX. Both of these defects are linked to the X chromosome and are typically passed from a healthy (carrier) mother to her male offspring, since males are XY. Females would need to inherit a defective gene from each parent to manifest the disease, since they are XX. Patients with hemophilia bleed from even minor internal and external wounds, and leak blood into joint spaces after exercise and into urine and stool. Hemophilia C is a rare condition that is triggered by an autosomal (not sex) chromosome that renders factor XI nonfunctional. It is not a true recessive condition, since even individuals with a single copy of the mutant gene show a tendency to bleed. Regular infusions of clotting factors isolated from healthy donors can help prevent bleeding in hemophiliac patients. At some point, genetic therapy will become a viable option.

In contrast to the disorders characterized by coagulation failure is thrombocytosis, also mentioned earlier, a condition characterized by excessive numbers of platelets that increases the risk for excessive clot formation, a condition known as thrombosis . A thrombus (plural = thrombi) is an aggregation of platelets, erythrocytes, and even WBCs typically trapped within a mass of fibrin strands. While the formation of a clot is normal following the hemostatic mechanism just described, thrombi can form within an intact or only slightly damaged blood vessel. In a large vessel, a thrombus will adhere to the vessel wall and decrease the flow of blood, and is referred to as a mural thrombus. In a small vessel, it may actually totally block the flow of blood and is termed an occlusive thrombus. Thrombi are most commonly caused by vessel damage to the endothelial lining, which activates the clotting mechanism. These may include venous stasis, when blood in the veins, particularly in the legs, remains stationary for long periods. This is one of the dangers of long airplane flights in crowded conditions and may lead to deep vein thrombosis or atherosclerosis, an accumulation of debris in arteries. Thrombophilia, also called hypercoagulation, is a condition in which there is a tendency to form thrombosis. This may be familial (genetic) or acquired. Acquired forms include the autoimmune disease lupus, immune reactions to heparin, polycythemia vera, thrombocytosis, sickle cell disease, pregnancy, and even obesity. A thrombus can seriously impede blood flow to or from a region and will cause a local increase in blood pressure. If flow is to be maintained, the heart will need to generate a greater pressure to overcome the resistance.

When a portion of a thrombus breaks free from the vessel wall and enters the circulation, it is referred to as an embolus . An embolus that is carried through the bloodstream can be large enough to block a vessel critical to a major organ. When it becomes trapped, an embolus is called an embolism. In the heart, brain, or lungs, an embolism may accordingly cause a heart attack, a stroke, or a pulmonary embolism. These are medical emergencies.

Among the many known biochemical activities of aspirin is its role as an anticoagulant. Aspirin (acetylsalicylic acid) is very effective at inhibiting the aggregation of platelets. It is routinely administered during a heart attack or stroke to reduce the adverse effects. Physicians sometimes recommend that patients at risk for cardiovascular disease take a low dose of aspirin on a daily basis as a preventive measure. However, aspirin can also lead to serious side effects, including increasing the risk of ulcers. A patient is well advised to consult a physician before beginning any aspirin regimen.

A class of drugs collectively known as thrombolytic agents can help speed up the degradation of an abnormal clot. If a thrombolytic agent is administered to a patient within 3 hours following a thrombotic stroke, the patient’s prognosis improves significantly. However, some strokes are not caused by thrombi, but by hemorrhage. Thus, the cause must be determined before treatment begins. Tissue plasminogen activator is an enzyme that catalyzes the conversion of plasminogen to plasmin, the primary enzyme that breaks down clots. It is released naturally by endothelial cells but is also used in clinical medicine. New research is progressing using compounds isolated from the venom of some species of snakes, particularly vipers and cobras, which may eventually have therapeutic value as thrombolytic agents.

Chapter Review

Hemostasis is the physiological process by which bleeding ceases. Hemostasis involves three basic steps: vascular spasm, the formation of a platelet plug, and coagulation, in which clotting factors promote the formation of a fibrin clot. Fibrinolysis is the process in which a clot is degraded in a healing vessel. Anticoagulants are substances that oppose coagulation. They are important in limiting the extent and duration of clotting. Inadequate clotting can result from too few platelets, or inadequate production of clotting factors, for instance, in the genetic disorder hemophilia. Excessive clotting, called thrombosis, can be caused by excessive numbers of platelets. A thrombus is a collection of fibrin, platelets, and erythrocytes that has accumulated along the lining of a blood vessel, whereas an embolus is a thrombus that has broken free from the vessel wall and is circulating in the bloodstream.

Interactive Link Questions

Clotting factors flow through the blood vessels in their inactive state. The endothelium does not have thrombogenic tissue factor to activate clotting factors.

Review Questions

Critical thinking questions.

1. A lab technician collects a blood sample in a glass tube. After about an hour, she harvests serum to continue her blood analysis. Explain what has happened during the hour that the sample was in the glass tube.

2. Explain why administration of a thrombolytic agent is a first intervention for someone who has suffered a thrombotic stroke.

Answers for Critical Thinking Questions

  • When blood contacts glass, the intrinsic coagulation pathway is initiated. This leads to the common pathway, and the blood clots. Within about 30 minutes, the clot begins to shrink. After an hour, it is about half its original size. Its heavier weight will cause it to fall to the bottom of the tube during centrifugation, allowing the lab technician to harvest the serum remaining at the top.
  • In a thrombotic stroke, a blood vessel to the brain has been blocked by a thrombus, an aggregation of platelets and erythrocytes within a blood vessel. A thrombolytic agent is a medication that promotes the breakup of thrombi.

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31.4 Blood Flow and Blood Pressure Regulation

Learning objectives.

In this section, you will explore the following questions:

  • How does blood flow through the body?
  • How is blood pressure regulated?

Connection for AP ® Courses

The information in this section is not within the scope for AP ® . However, the exchange of oxygen and carbon dioxide at capillary beds is an application of diffusion, a phenomenon we explored in detail in an earlier chapter. In addition, because many persons suffer from high blood pressure, often called the “silent killer,” you might find it informative to know how blood pressure is regulated and why lack of appropriate regulation is detrimental.

Blood pressure (BP) is the pressure exerted by blood on the walls of a blood vessel that helps to push blood through the body. Systolic blood pressure measures the amount of pressure that blood exerts on vessels while the heart is beating. The optimal systolic blood pressure is 120 mmHg. Diastolic blood pressure measures the pressure in the vessels between heartbeats. The optimal diastolic blood pressure is 80 mmHg. Many factors can affect blood pressure, such as hormones, stress, exercise, eating, sitting, and standing. Blood flow through the body is regulated by the size of blood vessels, by the action of smooth muscle, by one-way valves, and by the fluid pressure of the blood itself.

How Blood Flows Through the Body

Blood is pushed through the body by the action of the pumping heart. With each rhythmic pump, blood is pushed under high pressure and velocity away from the heart, initially along the main artery, the aorta. In the aorta, the blood travels at 30 cm/sec. As blood moves into the arteries, arterioles, and ultimately to the capillary beds, the rate of movement slows dramatically to about 0.026 cm/sec, one-thousand times slower than the rate of movement in the aorta. While the diameter of each individual arteriole and capillary is far narrower than the diameter of the aorta, and according to the law of continuity, fluid should travel faster through a narrower diameter tube, the rate is actually slower due to the overall diameter of all the combined capillaries being far greater than the diameter of the individual aorta.

The slow rate of travel through the capillary beds, which reach almost every cell in the body, assists with gas and nutrient exchange and also promotes the diffusion of fluid into the interstitial space. After the blood has passed through the capillary beds to the venules, veins, and finally to the main venae cavae, the rate of flow increases again but is still much slower than the initial rate in the aorta. Blood primarily moves in the veins by the rhythmic movement of smooth muscle in the vessel wall and by the action of the skeletal muscle as the body moves. Because most veins must move blood against the pull of gravity, blood is prevented from flowing backward in the veins by one-way valves. Because skeletal muscle contraction aids in venous blood flow, it is important to get up and move frequently after long periods of sitting so that blood will not pool in the extremities.

Blood flow through the capillary beds is regulated depending on the body’s needs and is directed by nerve and hormone signals. For example, after a large meal, most of the blood is diverted to the stomach by vasodilation of vessels of the digestive system and vasoconstriction of other vessels. During exercise, blood is diverted to the skeletal muscles through vasodilation while blood to the digestive system would be lessened through vasoconstriction. The blood entering some capillary beds is controlled by small muscles, called precapillary sphincters, illustrated in Figure 31.18 . If the sphincters are open, the blood will flow into the associated branches of the capillary blood. If all of the sphincters are closed, then the blood will flow directly from the arteriole to the venule through the thoroughfare channel (see Figure 31.18 ). These muscles allow the body to precisely control when capillary beds receive blood flow. At any given moment only about 5-10% of our capillary beds actually have blood flowing through them.

Visual Connection

  • Arteries have thicker smooth muscle layers to accommodate the changes in pressure from the heart.
  • Arteries carry plasma.
  • Arteries have thinner smooth muscle layers and valves and move blood by the action of skeletal muscle.
  • Arteries are thin walled.

Link to Learning

Visit this site to see the circulatory system’s blood flow.

Proteins and other large solutes cannot leave the capillaries. The loss of the watery plasma creates a hyperosmotic solution within the capillaries, especially near the venules. This causes about 85% of the plasma that leaves the capillaries to eventually diffuses back into the capillaries near the venules. The remaining 15% of blood plasma drains out from the interstitial fluid into nearby lymphatic vessels ( Figure 31.19 ). The fluid in the lymph is similar in composition to the interstitial fluid. The lymph fluid passes through lymph nodes before it returns to the heart via the vena cava. Lymph nodes are specialized organs that filter the lymph by percolation through a maze of connective tissue filled with white blood cells. The white blood cells remove infectious agents, such as bacteria and viruses, to clean the lymph before it returns to the bloodstream. After it is cleaned, the lymph returns to the heart by the action of smooth muscle pumping, skeletal muscle action, and one-way valves joining the returning blood near the junction of the venae cavae entering the right atrium of the heart.

Evolution Connection

Vertebrate diversity in blood circulation.

Blood circulation has evolved differently in vertebrates and may show variation in different animals for the required amount of pressure, organ and vessel location, and organ size. Animals with longs necks and those that live in cold environments have distinct blood pressure adaptations.

Long necked animals, such as giraffes, need to pump blood upward from the heart against gravity. The blood pressure required from the pumping of the left ventricle would be equivalent to 250 mm Hg (mm Hg = millimeters of mercury, a unit of pressure) to reach the height of a giraffe’s head, which is 2.5 meters higher than the heart. However, if checks and balances were not in place, this blood pressure would damage the giraffe’s brain, particularly if it was bending down to drink. These checks and balances include valves and feedback mechanisms that reduce the rate of cardiac output. Long-necked dinosaurs such as the sauropods had to pump blood even higher, up to ten meters above the heart. This would have required a blood pressure of more than 600 mm Hg, which could only have been achieved by an enormous heart. Evidence for such an enormous heart does not exist and mechanisms to reduce the blood pressure required include the slowing of metabolism as these animals grew larger. It is likely that they did not routinely feed on tree tops but grazed on the ground.

Living in cold water, whales need to maintain the temperature in their blood. This is achieved by the veins and arteries being close together so that heat exchange can occur. This mechanism is called a countercurrent heat exchanger. The blood vessels and the whole body are also protected by thick layers of blubber to prevent heat loss. In land animals that live in cold environments, thick fur and hibernation are used to retain heat and slow metabolism.

The heart of a newly discovered mammal species is asymmetric. The right side of the heart is smaller than the left side.

What is likely to be true about this species?

  • The right side of the heart sends blood to the lungs.
  • The right side of the heart sends blood to the body.
  • The right side of the heart sends blood to locations above the heart.
  • The right side of the heart sends blood to only the brain.

Blood Pressure

The pressure of the blood flow in the body is produced by the hydrostatic pressure of the fluid (blood) against the walls of the blood vessels. Fluid will move from areas of high to low hydrostatic pressures. In the arteries, the hydrostatic pressure near the heart is very high and blood flows to the arterioles where the rate of flow is slowed by the narrow openings of the arterioles. During systole, when new blood is entering the arteries, the artery walls stretch to accommodate the increase of pressure of the extra blood; during diastole, the walls return to normal because of their elastic properties. The blood pressure of the systole phase and the diastole phase, graphed in Figure 31.20 , gives the two pressure readings for blood pressure. For example, 120/80 indicates a reading of 120 mm Hg during the systole and 80 mm Hg during diastole. Throughout the cardiac cycle, the blood continues to empty into the arterioles at a relatively even rate. This resistance to blood flow is called peripheral resistance .

Blood Pressure Regulation

Cardiac output is the volume of blood pumped by the heart in one minute. It is calculated by multiplying the number of heart contractions that occur per minute (heart rate) times the stroke volume (the volume of blood pumped into the aorta per contraction of the left ventricle). Therefore, cardiac output can be increased by increasing heart rate, as when exercising. However, cardiac output can also be increased by increasing stroke volume, such as if the heart contracts with greater strength. Stroke volume can also be increased by speeding blood circulation through the body so that more blood enters the heart between contractions. During heavy exertion, the blood vessels relax and increase in diameter, offsetting the increased heart rate and ensuring adequate oxygenated blood gets to the muscles. Stress triggers a decrease in the diameter of the blood vessels, consequently increasing blood pressure. These changes can also be caused by nerve signals or hormones, and even standing up or lying down can have a great effect on blood pressure.

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  • Biology Article
  • What are Blood Vessels

What are Blood vessels?

The human circulatory system consists of the heart, blood cells, lymphatic system and network of blood vessels. These four main organs have specific roles and functions, which work together to keep us active and healthy.

Have you ever imagined what would happen if the blood vessels stopped functioning for a few seconds?

Yes, we would die from SCA – Sudden Cardiac Arrest.

Let’s learn more in detail about blood vessels and their types.

Angiology is the branch of anatomy or human science that deals with the study of the circulatory system, blood cells, arteries, veins and diseases related to the circulatory system.

Read more: Blood and Blood Vessels

Blood Vessels

The networks of hollow tubes like pipes, which carry blood to and from all parts of the body, are called blood vessels. These vessels carry blood in both the directions, i.e. one from the heart to all other parts and another from all body parts to the heart.

Types of Blood Vessels

The three types of blood vessels are:

Arteries are the main blood vessels that carry and transport oxygenated blood or oxygen-rich blood from the heart to other parts of the body. They are the strongest blood vessels with thicker walls and are muscular in nature. It consists of three distinct layers, which are rigid, thicker and highly muscular. Arteries are located deep within the body and are red in colour. These blood vessels are with high pressure and move in a downward direction from the heart to the body tissues.

Also refer: Why arteries have thick walls.

Veins are thin, tube-like elastic blood vessels, present closer to the surface of the skin. These translucent blood vessels are blue in colour and carry impure or deoxygenated blood from all parts of the body to heart. These blood vessels are with low pressure and move in an upward direction, i.e. from the cells, tissues and other organs to the heart. Compared to the arteries, veins are thin-walled.

Also refer: Difference between arteries and veins .

Capillaries

Short and tiny blood vessels, found within the tissues are called capillaries. Capillaries bring about the exchange of substances between blood and tissues. These blood vessels also function by connecting arterial systems to the venous system and help in exchange of substances across cells.

Recommended Video:

assignment of blood vessel

Layers of Blood Vessels

Both arteries and veins consist of three layers.

  • Tunica Intima : It is the innermost and thinnest layer of arteries and veins, which have direct contact with the blood flow.
  • Tunica Media : It is the middle layer of an artery or vein, which is made up of smooth muscle cells.
  • Tunica Externa: It is present adjacent to the tunica media and is composed of collagen and functions by supporting the elastic lamina in arteries. It is also known as tunica adventitia .

Explore more: Blood and the Circulatory System

Functions of Blood Vessels

  • Blood vessels play a vital role in the gaseous exchange.
  • Blood vessels help maintain a constant internal temperature of an organism.
  • The vital function of the blood vessels is protecting against the loss of blood during injuries.
  • Blood vessels are also involved in circulating both oxygenated (poor) and deoxygenated (impure) blood from and to the heart.
  • Blood vessels help in the transportation of nutrients, water, minerals, hormones and all other essential components required for the different body metabolism.

Frequently Asked Questions

What are the functions of blood vessels.

The blood vessels are channels through which blood is distributed and collected from the entire body to and from the heart.

What are the 3 types of blood vessels?

The three types of blood vessels are arteries, veins and capillaries.

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April 26, 2024

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Coordinating blood vessel activity may be associated with better brain performance

by Tohoku University

Coordinating blood vessel activity may be associated with better brain performance

Compared with computers, the brain can perform computations with a very low net energy supply. Yet our understanding surrounding how the biological brain manages energy is still incomplete. What is known, however, is that the dilation and constriction cycles of blood vessels, or vasomotion, spontaneously occur in the brain, a process that likely contributes to enhancing the circulation of energetic nutrients and clearing wasteful materials.

Researchers from Tohoku University have developed a method that easily observes and monitors blood vessel dynamics in the mouse brain . This can be done either through the intact skull of a mouse, or deep into the brain using an implanted optical fiber.

The findings were detailed in the journal, eLife , on April 17, 2024.

Since it has been reported that sensory stimuli can cause dilation of blood vessels or hyperemia, researchers sought to induce vasomotion via presenting mice with visual stimuli . What they discovered was when a mouse was shown a horizontally moving stripe pattern that changed direction every two to three seconds, it caused a reaction in the mouse's blood vessels that matched the pattern's speed.

Mice were presented with 15-minute visual training sessions interleaved with one-hour resting periods for four times per day. With such spaced training, the amplitude of the synchronized vasomotion gradually increased. Interestingly, the visually induced vasomotion was not confined to the area of the cerebral cortex responsible for visual information processing. In other words, synchronized vasomotion spread throughout the whole brain.

"Synchronized vascular motion can be entrained with slowly oscillating visual stimuli," says Professor Ko Matsui of the Super-network Brain Physiology lab at Tohoku University, who led the research. "Such enhancement of circulation mechanisms may benefit the information processing capacity of the brain."

While it's long been known that changes in neuron connections support learning and memory, the plasticity of vasomotion hasn't been described before. Matsui and his colleagues found that a specific visual pattern makes the eyes move more, and this eye movement improvement depends on changes in the brain's cerebellum. The researchers also observed that blood vessel activity in the cerebellum synchronized with this optokinetic motor learning.

Lead study investigator, Daichi Sasaki, believes that synchronized vasomotion, which efficiently delivers oxygen and glucose, could improve learning abilities.

He states, "Our next step is to explore the advantages of vasomotion synchronization. It might help clear waste like amyloid beta , potentially delaying or preventing dementia. Stroke recovery could also benefit from better energy supply and waste removal. Additionally, synchronized vasomotion might even enhance intelligence beyond our natural capabilities."

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COMMENTS

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    A vein is a blood vessel that conducts blood toward the heart. Compared to arteries, veins are thin-walled vessels with large and irregular lumens (see Figure 20.7). Because they are low-pressure vessels, larger veins are commonly equipped with valves that promote the unidirectional flow of blood toward the heart and prevent backflow toward the ...

  2. 20.2: Structure and Function of Blood Vessels

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  12. PDF The Circulatory System: Blood Vessels

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  16. 31.4 Blood Flow and Blood Pressure Regulation

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  21. Ch 20 Blood vessels Assignment Flashcards

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