Biomedical Engineering Reference
In-Depth Information
constriction or dilation. It is known that there are communicating junctions between endo-
thelial cells and vascular smooth muscle cells that help to regulate changes in the diameter
of the blood vessel. However, we also know that vasoactive compounds are released into
the bloodstream. Therefore, neither theory represents the physiology completely.
There are two other theories about local blood flow regulation that are based on the
pressure changes that can occur within the blood vessel. Imagine an increase in arterial
blood pressure. This would be accompanied with an increase in blood flow to the tissue,
causing an increased oxygen/nutrient delivery to the tissue. It has been experimentally
shown that within a minute, this increase in blood flow returns back to normal levels in a
process termed autoregulation of blood flow. The first theory, the metabolic theory, pro-
poses that an increased oxygen/nutrient delivery causes constriction of the blood vessels
in much the same way that was discussed previously. Increased oxygen (or nutrients)
causes an increase in cellular by-products to be released within the vascular network (or
within endothelial cells) which directly communicates with precapillary sphincters, caus-
ing a constriction. The second theory, the myogenic theory, suggests that it is not cellular
compounds that regulate blood flow. Instead, the constriction of blood vessels is caused
by the pressure-induced stretch of the blood vessels. It has been observed that after blood
vessels experience a small sudden stretch, the vascular smooth muscle cells start to con-
strict to counter the stretch. Also, when the pressure reduces in the blood vessels, the
diameter suddenly reduces, causing a relaxation of the vascular smooth muscle cells to
counter the decreased pressure forces. Either of these changes has the net effect of bringing
the vessel back to its normal resting state. It is likely that some combination of all of these
mechanisms is responsible for the local control of blood vessel diameter.
We will now briefly discuss the humoral regulation of blood vessel diameter. Three of
the most potent vasoconstrictors are vasopressin, angiotensin, and norepinephrine.
Vasopressin works in conjunction with the kidneys to increase water absorption by decreas-
ing the flow through the circulatory system. Angiotensin acts to increase the vascular resis-
tance of all of the arterioles within a specific tissue upon release. This effectively decreases
blood flow through the tissue. During stress situations, norepinephrine is released and can
partially regulate blood flow to areas of need by shunting blood away from areas with a
lower need. Two of the most potent vasodilators are the super-family of kinins and hista-
mine. Both of these compounds have direct roles in the inflammatory response by increas-
ing vascular flow to an inflamed region. Also, these compounds increase the permeability
of the capillaries to allow for the rapid extravasation of white blood cells.
6.4 PRESSURE DISTRIBUTION THROUGHOUT
THE MICROVASCULAR BEDS
The pressure gradient across microvascular beds has been proved to be one of the most
critical fluid parameters in regulating the flow throughout these vessels (the fluid velocity
is so slow in these vessels that small changes in the pressure can cause large changes in
the flow conditions, including velocity, shear stress, and shear rate). The pressure gradient
across microvascular beds has been experimentally measured using two flow probes
inserted into various branches along the network. By knowing the distance between these
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