Special Circulations

In this section, we address how blood flow regulation in several representative organs illustrates the principles discussed above and we also describe the additional features of blood flow control that are unique to certain tissues and conditions (fetus).

Coronary Circulation

The coronary circulation must deliver O2 at a rate that keeps pace with cardiac demand. Under resting conditions, blood flow to the heart is about 70 mL/min per 100 g, and it increases five- to sixfold during maximal cardiac work. Blood flow in the left ventricle is about 80 mL/min per 100 g, which is twice the flow in the right ventricle and four times the flow in the atria. Myocardial O2 consumption is also very high (8 mL/min per 100 g) at rest (which is 20 times the resting value in skeletal muscle), and it increases about fivefold during maximal cardiac work.

Blood flow to the heart is governed almost entirely by intrinsic factors. The rate of O2 use by the myocardium is proportional to cardiac work; hence, factors such as systolic pressure (afterload), heart rate, and stroke volume all influence myocardial O2 consumption. As cardiac work increases, the elevated metabolic activity results in dilation of the coronary arterioles, thus increasing blood flow to heart muscle (active hyper-emia). The coronary vasculature normally exhibits excellent pressure flow autoregulation and brisk reactive hyperemias. Hormones and neurotransmitters exert only a small direct influence on the coronary blood flow because of the low density of receptors on coronary vessels. The low density of adrenergic receptors enables the heart to respond to sympathetic stimulation with vasodilation. Although sympathetic nerves would ordinarily tend to constrict coronary arteries, the increased cardiac work that accompanies sympathetic stimulation also results in an elevated O2 demand. Thus, the feeble vasoconstriction elicited by «-adrenergic stimulation is easily overridden by the corresponding metabolic vaso-dilation. The opposite scenario is seen with vagal stimulation. Although acetylcholine tends to directly dilate the coronary arterioles, cholinergic stimulation reduces cardiac O2 demand by slowing the heart rate. Here again, metabolic factors dominate coronary vascular tone and the result of vagal stimulation is a reduction in blood flow.

Although the average flow through the coronary circulation is regulated by intrinsic factors, the moment-to-moment flow of blood through the coronary vessels is strongly influenced by the mechanical activity of the heart. Figure 6 demonstrates the mechanical effects on coronary blood flow. When the left ventricle starts to

Skewed Right Mean Median

FIGURE 6 Blood flow through the left coronary artery and aortic pressure during the cardiac cycle. With the onset of ventricular contraction (from just before the first dashed line), blood flow decreases sharply as the coronary vessels are compressed by the ventricular muscle. During the ejection phase (between the dashed lines), only minimal flow occurs. Most coronary flow occurs during ventricular relaxation (from the second dashed line on). Flow is highest in early diastole when perfusion pressure is high and compressive forces are low.

FIGURE 6 Blood flow through the left coronary artery and aortic pressure during the cardiac cycle. With the onset of ventricular contraction (from just before the first dashed line), blood flow decreases sharply as the coronary vessels are compressed by the ventricular muscle. During the ejection phase (between the dashed lines), only minimal flow occurs. Most coronary flow occurs during ventricular relaxation (from the second dashed line on). Flow is highest in early diastole when perfusion pressure is high and compressive forces are low.

contract, flow through the left coronary arteries falls abruptly and, under conditions of increased contractility, may even reverse for a brief period. This reduction of flow is due to compression of the coronary vessels that pass through the left ventricular muscle. During the ejection period of the cardiac cycle, the aortic pressure is rising and some forward flow occurs. The compressional forces are highest near the endocardium and diminish near the epicardium. As a result, coronary flow during systole is nonuniformly distributed across the heart wall, with almost no blood flow reaching the inner layers. Figure 6 also reveals that most of the coronary flow takes place during early diastole; when the ventricular muscle is relaxed, the mechanical compression forces are low and aortic pressure is still high. At this time, the blood flow gradient across the ventricular wall reverses, with the inner muscle layers receiving most of the flow. Although a similar pattern of blood flow changes is observed in the right coronary artery during the cardiac cycle, the changes in flow to the right ventricle are relatively small because the compression forces generated in the right ventricle during systole are comparably small.

It is interesting that the average blood flow over the entire cardiac cycle is uniformly distributed across the wall of the left ventricle. Although the intrinsic mechanisms are too slow to keep blood flow constant through the cardiac cycle, they can adjust flow so that the average flow meets the metabolic needs of the myocardium. To compensate for the blood flow deficit during each systole, the arterioles in the inner layers are simply kept in a more dilated state so these muscles will be compensated with extra perfusion during each diastole. Unfortunately, this compensatory response diminishes the dilatory reserve of the inner muscle layers, and as a result the subendocardium is always the most vulnerable to ischemia whenever the coronary arteries are obstructed, as occurs in coronary artery disease.

Another unique feature of the coronary circulation is the high O2 extraction normally seen across this vascular bed. The myocardium extracts >80% of the O2 from coronary blood, which compares with the whole body average of 25% at rest. The high O2 extraction can be attributed to the great demand of this tissue for O2 under resting conditions. It is not surprising, therefore, that all capillaries are open to perfusion in the resting myocardium. In other organs (e.g., skeletal muscle), recruitment of additional perfused capillaries is an important mechanism for enhancement of O2 delivery by both increasing the surface area available for O2 exchange and by reducing the diffusion distance for O2 between the blood and myocytes. The high O2 extraction in the heart would indicate that this tissue is on the verge of underperfusion. However, because of the tight coupling of coronary blood flow with oxidative metabolism, the O2 requirements of the heart always appear to be precisely met by changes in blood flow. Of the chemical factors that have been invoked to explain metabolic vasodilation, adenosine has received the most attention in the heart.

If coronary blood flow is interrupted, myocardial ischemia will quickly ensue. The heart normally oxidizes fatty acids and lactate as its energy source. However, in the absence of O2, cardiac myocytes switch to anaerobic glycolysis (using its glycogen store), which is inefficient and cannot maintain energy balance. Within 30 sec, lactic acid buildup results in cellular acidosis, while the accumulation of inorganic phosphate inhibits the function of actin-myosin filaments. A consequence of these cellular events is an inhibition of muscle contraction that occurs almost immediately after cessation of blood flow. Although ATP falls at a relatively slow rate, such that the myocytes will not begin to die until after at least 20 min of severe ischemia, the loss of mechanical function of the heart can be disastrous. If only a small branch of the coronary system is involved, the remaining well-perfused myocardium can maintain cardiac output. If a major branch is involved, however, the ventricle can be so compromised that blood pressure will fall, rendering the rest of the heart ischemic, and circulatory collapse will soon follow. In this positive feedback situation, death of the individual quickly ensues.

Collateral vessels connect adjacent branches of coronary arteries so that occlusion of one arterial branch, as occurs in a heart attack, does not completely stop blood flow to the affected tissue. Some animals, such as the guinea pig, have well-developed collaterals and occlusion of a coronary branch is tolerated with no tissue necrosis. Other animals such as the pig have few collaterals and the same occlusion will result in infarction (death of tissue) of the entire downstream region. Humans are somewhere between these two extremes. If the occlusion of a coronary branch is gradual in onset, that is, over weeks and months, the collateral vessels will actually grow in response to the decreased blood flow. It is not known what factors mediate collateral growth, but it is probably related to the synthesis and release of angiogenic factors (e.g., adenosine) from underperfused tissue. Some coronary patients have such well-developed collateral vessels that an entire arterial branch may be completely occluded without compromising blood flow to the muscle tissue that would normally be perfused from that branch.

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