JF Venules and Veins

Venules (ven'├╝lz) are the microscopic vessels that continue from the capillaries and merge to form veins. The veins, which carry blood back to the atria, follow pathways that roughly parallel those of the arteries.

The walls of veins are similar to those of arteries in that they are composed of three distinct layers. However, the middle layer of the venous wall is poorly developed. Consequently, veins have thinner walls that contain less smooth muscle and less elastic tissue than those of comparable arteries, but their lumens have a greater diameter (figs. 15.24 and 15.31).

(a) Venous valves allow blood to move toward the heart but

(b) prevent blood from moving backward away from the heart.

(a) Venous valves allow blood to move toward the heart but

(b) prevent blood from moving backward away from the heart.

Many veins, particularly those in the upper and lower limbs, contain flaplike valves (called semilunar valves), which project inward from their linings. Valves, shown in figure 15.32, are usually composed of two leaflets that are pushed closed if the blood begins to back up in a vein. These valves aid in returning blood to the heart because they are open as long as the flow is toward the heart but close if it is in the opposite direction.

Veins also function as blood reservoirs, useful in times of blood loss. For example, in hemorrhage accompanied by a drop in arterial blood pressure, sympathetic nerve impulses reflexly stimulate the muscular walls of the veins. The resulting venous constrictions help maintain blood pressure by returning more blood to the heart. This mechanism ensures a nearly normal blood flow even when as much as 25% of the blood volume is lost. Figure 15.33 illustrates the relative volumes of blood in the veins and other blood vessels.

Table 15.3 summarizes the characteristics of blood vessels. Clinical Application 15.3 examines disorders of blood vessels.

Blood Vessel Disorders

In the arterial disease atherosclerosis, deposits of fatty materials, particularly cholesterol, are formed within the intima and inner lining of the arterial walls. Such deposits, called plaque, protrude into the lumens of the vessels and interfere with blood flow (fig. 15E). Furthermore, plaque often forms a surface texture that can initiate formation of a blood clot, increasing the risk of developing thrombi or emboli that cause blood deficiency (ischemia) or tissue death (necrosis) downstream from the obstruction.

The walls of affected arteries may degenerate, losing their elasticity and becoming hardened or sclerotic. In this stage of the disease, called arteriosclerosis, a sclerotic vessel may rupture under the force of blood pressure.

Risk factors for developing atherosclerosis include a fatty diet, elevated blood pressure, tobacco smoking, obesity, and lack of physical exercise. Emotional and genetic factors may also increase susceptibility to atherosclerosis (see chapter 18).

If atherosclerosis so weakens the wall of an artery that blood pressure dilates a region of it, a pulsating sac called an aneurysm may form. Aneurysms tend to grow. If the resulting sac develops by a longitudinal splitting of the middle layer of the arterial wall, it is called a dissecting aneurysm. An aneurysm may cause symptoms by pressing on nearby organs, or it may rupture and produce a great loss of blood.

Aneurysms may also result from trauma, high blood pressure, infections, inherited disorders such as Marfan syndrome, or congenital defects in blood vessels. Common sites of aneurysms include the thoracic and abdominal aorta and an arterial circle at the base of the brain (circle of Willis).

Phlebitis, or inflammation of a vein, is relatively common. It may occur in association with an injury or infection or after surgery, or it may develop for no apparent reason.

If inflammation is restricted to a superficial vein, such as the greater or lesser saphenous veins, blood flow may be rechanneled through other vessels. But if it occurs in a deep vein, such as the tibial, peroneal, popliteal, or femoral veins, the consequences can be quite serious, particularly if the blood within the affected vessel clots and blocks normal circulation. This condition, called thrombophlebitis, introduces a risk that a blood clot within a vein will detach, move with the venous blood, pass through the heart, and lodge in the pulmonary arterial system within a lung. Such an obstruction is called a pulmonary embolism.

Varicose veins are abnormal and irregular dilations in superficial veins, particularly in the legs. This condition is usually associated with prolonged, increased back pressure within the affected vessels due to gravity, as occurs when a person stands. Crossing the legs or sitting in a chair so that its edge presses against the area behind the knee can obstruct venous blood flow and aggravate varicose veins.

Increased venous back pressure stretches and widens the veins. Because the valves within these vessels do not change size, they soon lose their abilities to block the backward flow of blood, and blood tends to accumulate in the enlarged regions.

Increased venous pressure is also accompanied by rising pressure within the venules and capillaries that supply the veins. Consequently,

How does the structure of a vein differ from that of an artery?

What are the functions of veins and venules?

How does venous circulation help to maintain blood pressure when hemorrhaging causes blood loss?

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Essentials of Human Physiology

Essentials of Human Physiology

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