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Blood Vessels

The Flow of Blood through Blood Vessels

Blood vessels form a tubular network that allows blood to travels from the heart to the tissues and back to the heart again. Blood that leaves the heart passes into arteries. Large arteries branch into progressively smaller arteries that function to deliver blood to various regions of the body. Small arteries branch into even smaller vessels called arterioles, which function to regulate the flow of blood into different tissues. Arterioles branch into capillaries, the smallest of all blood vessels. Capillaries are the sites of nutrient and waste exchange between the blood and body cells. Capillaries are microscopic vessels that join the arterial system with the venous system. Blood coming out of the capillaries passes into vessels of increasing diameter as it flows back toward the heart. Capillaries join to form venules, which then merge to form small veins. Small veins unite to form large veins that eventually deliver blood back to the heart.



Arteries serve as (1) efficient conduits for the movement of blood and (2) pressure reservoirs that keep blood moving during diastole. Arteries have a large internal diameter and thus offer little resistance to the flow of blood. Arteries also contain an elastic layer in their walls. Elastin is a protein fiber that has elastic qualities. During systole, large arteries distend with blood as their elastic walls stretch. During diastole, the walls rebound, thus pushing blood along. In this way the arteries act as a pressure reservoir that maintains a constant flow of blood through the capillaries despite pressure fluctuation during the cardiac cycle. Arteries also have a smooth muscular layer that functions to regulate the flow of blood through the artery. Contraction of the smooth muscle decreases the internal diameter of the vessel in a process called vasoconstriction. Relaxation of the smooth muscle increases the intermnal diameter in a process called vasodilation.



Arterioles serve as (1) the major determinant of blood pressure and (2) as the major determinant of blood flow to the individual organs Arterioles have a much smaller diameter than arteries and thus provide significant resistance to the flow of blood. This resistance creates pressure in the circulatory system. Pressure is required to provide adequate flow of blood to all parts of the body. Blood flow to individual organs can be regulated by controlling the diameter of the arterioles. Vasodilation of an arteriole lowers resistance and results in an increase in flow through that particular arteriole. Vasoconstriction of an arteriole increases resistance and results in decreased flow through that particular arteriole.



Capillaries are the smallest and most numerous of blood vessels. Capillaries function as the site of exchange of nutrients and wastes between blood and tissues. The anatomy of capillaries is well suited to the task of efficient exchange. Capillary walls are composed of a single layer of epithelial cells surrounded by a basement layer of connective tissue. The thin nature of the walls facilitates efficient diffusion of oxygen and carbon dioxide. Most capillaries also have pores between cells that allow for bulk transport of fluid and dissolved substances from the blood into the tissues and visa versa.

Although capillaries are extremely numerous (40 billion in the body), collectively they hold only about 5% of the total blood volume at any one time. This is because most capillaries are closed most of the time. Precapillary sphincters, which are bands of smooth muscle that wrap around arterioles, control the amount of blood flowing in a particular capillary bed. Contraction of the sphincter shuts off blood flow to a capillary bed, while relaxation of the sphincter allows blood to flow.



Veins are larger and more compliant (stretchable) than arteries, thus they can hold more blood. In fact, the veins act somewhat like a blood reservoir, containing 60% of the total blood volume at rest. As physical activity increases, the veins undergo vasoconstriction, driving more blood back to the heart and increasing circulation. Also, the return of venous blood to the heart is aided by one-way valves that insure unidirectional flow of blood.

Return of Venous Blood to the Heart

By the time blood has passed from the capillaries into the venous system the pressure has dropped significantly. The average blood pressure in the venous system is only 2 mmHg (millimeters of mercury) as compared to an average of 100 mmHg in the arterial system. The low venous pressure is barely adequate to drive blood back to the heart, particulary from the legs. Other mechanisms are needed to aid in the return of blood to the heart. The flow of venous blood back to the heart is increased by (1) the sympathetic nervous system, (2) the skeletal muscle pump, and (3) the respiratory pump.

Veins are enervated by sympathetic motor neurons. Sympathetic input causes vasoconstriction, which increases pressure, which drives blood back to the heart. When the body needs to mobilize more blood for physical activity, the sympathetic nervous system induces vasoconstriction of veins.

The figure to the right illustrates the action of the skeletal muscle pump. Veins pass between skeletal muscles.The contraction of skeletal muscle squeezes the vein, thus increasing blood pressure in that section of the vein. Pressure causes the upstream valve (furthest from the heart) to close and the downstream valve (the one closest to the heart) to open. Repeated cycles of contraction and relaxation, as occurs in the leg muscles while walking, effectively pumps blood back to the heart.

While the contraction of skeletal muscle in the legs drives venous blood out of the lower limbs, the act of breathing helps to drive venous blood out of the abdominal cavity. As air is inspired, the diaphragm descends and abdominal pressure increases. The increasing pressure squeezes veins and moves blood back toward the heart. The rhythmic movement of venous blood causes by the act of breathing is called the respiratory pump.



Atherosclerosis is the major cause of coronary artery disease and stroke. It is a progressive, degenerative disease that leads to the occlusion of small arteries. Blood flow through effected arteries is diminished and may eventually become completely blocked. Occlusion of the artery is due to the development of a fatty plaque. The plaque protrudes into the lumen (open space) of the artery, thus diminishing blood flow in the artery.

The formation of plaques occurs in a sequential fashion. First, cholesterol-rich lipids (fat) infiltrate the epithelium and are deposited within the wall of a blood vessel. Next, abnormal smooth muscle cells migrate to the site of the developing plaque, causing a bulge that narrows the lumen of the artery. This is followed by the formation of a connective tissue cap (scar tissue) over the developing plaque. Eventually the plaque becomes hardened by deposition of calcium salts.

If the endothelium overlying the plaque can become damaged (ulceration) the plaque may rupture, thus exposing the blood to the interior of the plaque. Connective tissue (collagen) in the plaque can stimulate the activation of platelets, thus leading to the formation of a blood clot. If the clot remains in place it is called a thrombus. If the clot breaks away and travels to another site it is called an embolus. The formation of a blood clot can lead to sudden occlusion of an artery. Occlusion of a coronary artery may lead to heart attack (myocardial infarction), while occlusion of a artery in the brain can lead to stroke.

Drugs that dissolve clots (clot busters) are used as treatment for acute myocardial infarction and stroke. Tissue plasminogen activator (TPA) is a human protein that facilitates the breakdown of blood clots. The gene that encodes TPA was cloned by a local biotechnology company, Amgen. Recombinant TPA is now available as a clinical drug. Although its expensive ($2000 dollars per dose), its very effective at breaking blood clots and saving lives. After Amgen looses its patent on TPA (15 years) the drug price will drop significantly. Streptokinase is another enzyme that dissolves blood clots. This not a human enzyme, but rather a streptococcus bacterial enzyme. Streptokinase is purified out of bacteria and packaged in pure form. Streptokinase is cheap ($2 dollars per dose) and effective, but may only be used a few times before the immune system renders it ineffective.


Risk Factors for Atherosclerosis

The cause of Atherosclerosis is not entirely clear. However there are certain risk factors that increase (statistically) one's chances of acquiring the disease. Risk factors for atherosclerosis include:

  1. genetic predisposition
  2. obesity
  3. age
  4. smoking
  5. hypertension
  6. diabetes
  7. high cholesterol

Of all the risk factors, high blood levels of cholesterol are the most significant. Cholesterol (shown as a yellow dot in the figure below) is an essential steroid. It is found in the plasma membrane of all cells and is the precursor to all steroid hormones. Blood levels of cholesterol are regulated by the liver. If cholesterol is absent from the diet, then the liver will synthesize it from fatty acids (red squares in figure below). If blood levels of cholesterol are excessive then the liver will secrete it into bile, which is then delivered to the small intestine and eliminated with the feces.

Because cholesterol is a lipid, it does not dissolve into the aqueous fluid of the blood. Cholesterol is transported in the blood bound to lipoproteins, which are soluble in the blood. LDLs (low-density lipoproteins) carry cholesterol from the liver to the cells. HDLs (high-density lipoproteins) carry cholesterol from the cells to the liver for excretion. High levels of LDL correlate with a higher incidence of atherosclerosis. This may be because the liver is sending too much cholesterol out into the body. Thus LDL is considered the "bad" cholesterol. High levels of HDL are correlated with a lower incidence of atherosclerosis. This may be because HDLs function to send cholesterol back to the liver for excretion, effectively lowering blood cholesterol. Thus HDL is considered the "good" cholesterol.

LDLs that have been oxidized by free radicals (highly reactive electron-deficient molecules) are considered to be the "worst" cholesterol. Antioxidants are chemicals that "soak up" free radicals before they can do much harm. Dietary intake of antioxidants, such as vitamin E, vitamin C, and beta-carotene has been shown to slow plaque deposition.

One can significantly lower blood levels of cholesterol, and therefore lower the risk of developing atherosclerosis, by limiting dietary intake of cholesterol. Also, absorption of dietary cholesterol can be limited by eating indigestible fibers such as oat bran, which inhibits the uptake of cholesterol from the food in the small intestine.


Coronary Artery Disease

Although a tremendous amount of blood flows through the chambers of the heart, this blood does not nourish the heart. The heart is nourished by blood from the coronary circulation, a system of arteries, capillaries and veins that brings blood to all of the tissues of the heart. As one begins to exercise, the heart works harder and therefore requires more oxygen. As oxygen demands of the heart increase, vasodilation of coronary arteries supplies more blood, thus meeting the demand.

Normally, coronary blood flow can keep pace with increased oxygen demands during exercise. However, if the coronary arteries are partially blocked by atherosclerotic plaques, as is observed in coronary artery disease, then blood flow through the coronary arteries may not be sufficient to supply the level of oxygen required. In this case, myocardial cells may experience ischemia (lack of oxygen). In the absence of oxygen cardiac cells shift to anaerobic respiration of glucose and produce lactic acid as a by-product. Lactic acid is thought to stimulate pain receptors. This pain in the chest, due to ischemia, is referred to as Angina Pectoris. The symptoms of angina pectoris reoccur whenever oxygen demand out-paces oxygen supply, for example, during exercise or stress. Vasodilators, such as nitroglycerin, are effective in treating angina pectoris because they open blood vessels occluded by plaques. Treatment for severe coronary artery disease is bypass surgery. In this procedure, a healthy artery, removed from a different part of the body, is grafted from the aorta to a region of the artery just downstream of the occlusion.


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(Revised September 17 1999)
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