Steven S. Segal
In the preceding chapters, we considered blood flow to peripheral capillary beds as if the “periphery” were a single entity. In this chapter, we break that entity down into some of its component parts. Because each organ in the body has its own unique set of requirements, special circulations within each organ have evolved with their own particular features and regulatory mechanisms. Especially for times of great stress to the body, each organ possesses circulatory adaptations that allow it to make the changes appropriate for causing minimal harm to the overall organism. Here, we focus on the circulations of the brain, heart, skeletal muscle, abdominal viscera, and skin. Elsewhere we discuss other special circulations in the context of particular organs—the lungs (see pp. 683–689), the kidneys (see pp. 745–750), the placenta (see pp. 1136–1139), and the fetal circulation (see pp. 1157–1158).
The blood flow to individual organs must vary to meet the needs of the particular organ, as well as of the whole body
The blood flow to each tissue must meet the nutritional needs of that tissue's parenchymal cells, while at the same time allowing those cells to play their role in the homeostasis of the whole individual. The way in which the circulatory system distributes blood flow must be flexible so that changing demands can be met. In the process of meeting these demands, the body makes compromises. Consider the circulatory changes that accompany exercise. Blood flow to active skeletal muscle increases tremendously through both an increase in and a redistribution of cardiac output. Blood flow to the coronary circulation must also rise to meet the demands of exercise. Furthermore, in order to dispose of the heat generated during exercise, the vessels in the skin dilate, thereby promoting heat transfer to the environment. As cardiac output is increasingly directed to active muscle and skin, circulation to the splanchnic and renal circulations decreases, while blood flow to the brain is preserved.
This chapter focuses on the perfusion of select systemic vascular beds, but keep in mind that the lungs receive the entire cardiac output and therefore must also be able to accommodate any changes in total blood flow.
Neural, myogenic, metabolic, and endothelial mechanisms control regional blood flow
Several mechanisms govern vascular resistance and thus the distribution of blood circulating throughout the body. The interplay among neural, myogenic, metabolic, and endothelial mechanisms establishes a resting level of vasomotor tone. The extent to which a particular vascular bed depends on a particular blood-flow-control mechanism varies from organ to organ. We have discussed the following four mechanisms in the preceding chapters, and briefly review them here.
The resistance vessels of nearly every organ are invested with fibers of the autonomic nervous system (ANS), particularly those of the sympathetic division (see pp. 542–543). In addition to playing a critical role in controlling blood pressure and cardiac output, the ANS modulates local blood flow to meet the needs of particular tissues.
Many vessels, particularly the muscular arteries and arterioles that govern vascular resistance, are inherently responsive to changes in transmural pressure. Increased pressure and the accompanying stretch of vascular smooth-muscle cells (VSMCs) elicit vasoconstriction (see pp. 477–478), whereas decreased pressure elicits vasodilation. This myogenic response plays an important role in the autoregulation (see p. 481) that occurs in the vessels of the brain, heart, skeletal muscle, and kidneys.
Throughout the body, the vessels that govern blood flow are sensitive to the local metabolic needs of parenchymal cells. Table 20-9 lists several changes that act synergistically to increase local blood flow. For example, a decrease in or pH promotes relaxation of VSMCs, thereby causing vasodilation. In response to activity, excitable cells raise extracellular K+ concentration ([K+]o), which also causes vasodilation. Tissues with high energy demands—such as the brain, heart, and skeletal muscle during exercise—rely heavily on such local control mechanisms.
Endothelial cells release a variety of vasoactive substances (see Table 20-10). For example, the shear stress exerted by the movement of blood through the vessel lumen stimulates the release of nitric oxide (NO), which relaxes VSMCs and prevents leukocyte adhesion. Endothelial cells and VSMCs also use gap junctions for electrical and chemical signaling between themselves, thereby coordinating their activity during blood flow control.
In addition to the previous mechanisms, which are part of a sophisticated feedback control system, other factors—which are not regulatory in nature—can affect the local circulation. These other factors are all mechanical forces that are external to the blood vessels and that tend to either to collapse or to open them. For example, in the heart (see p. 517) and skeletal muscle (see p. 517), muscle contraction transiently halts blood flow by compressing blood vessels within the tissue.