Biomedical Engineering Reference
In-Depth Information
the amount of blood needed would exceed the work capacity of the heart and nutrient
delivery would not be effective. Also, as tissues do not store oxygen, most of the excess
oxygen would go to “waste” and would be expelled out through the lungs. Therefore,
under normal conditions, the blood supply to all tissues meets the minimum requirements
of the tissue and no more than that.
In general, there are two mechanisms to control blood flow to tissues. The first mecha-
nism is an acute local control, which accounts for rapid constriction or dilation of the
blood vessels. The second control system is a long-term control, which leads to changes in
the number of blood vessels and/or the resting size (diameter/length) of the blood vessel.
We will restrict our discussion to the rapid acute control mechanism.
As mentioned before, the first major regulator of blood flow is the tissue oxygenation
level. When the quantity of oxygen in the blood or the quantity of oxygen within the tissue
reduces, there is a noticeable increase in the blood flow to that tissue. The rate of blood
flow increase is almost inversely proportional to the percentage of oxygen within the arte-
rial blood. At a level of 50% of the normal oxygen concentration, the blood flow increases
by approximately 2 times. At a level of 25% of the normal oxygen concentration, the blood
flow increases by slightly more than 3 times. Be cautioned though that this is not a linear
relationship. The first possible mechanism that regulates increased blood flow under
decreased arterial oxygen concentration is an increased vascular adenosine concentration
to act as a vasodilator (other vasodilators such as carbon dioxide, nitric oxide, and hydro-
gen ions, among others, can follow the same mechanism, but currently it is unknown
which of these vasodilators is the most important). Due to a decreased availability of oxy-
gen, the surrounding tissues release adenosine (or other dilators) into the bloodstream.
These dilators cause the vascular smooth muscle cells to relax and effectively increase
blood flow to that tissue by increasing flow through the capillary network. One problem
with this theory is that the vasodilator which is released into the blood capillaries would
have to diffuse against the blood flow (i.e., upstream) to the arterioles/precapillary sphinc-
ters to have a substantial effect on blood flow changes. Therefore, this mechanism cannot
account for all of the vascular changes seen in response to low tissue oxygenation.
A second common thought is that low oxygen concentration itself can directly induce
changes in the diameter of blood vessels. There is some evidence for this mechanism as
well, but the same problem about downstream sensing receptors and the communication
to the upstream vascular smooth muscle cells is associated with this theory. However, a
better theory would include some combination of these mechanisms. Some microcircula-
tory research groups have experimental results that suggest that there is a rapid communi-
cation between the endothelial cells that form the capillaries and those that line the
metarterioles. This communication exists through the presence of gap junctions between
cells. In a similar manner to the above theory, when oxygen (or other nutrients) concentra-
tion decreases within the tissue supplied by the capillary beds, by-products of cellular res-
piration, or other vaso-active compounds can be formed within endothelial cells. These
compounds can then be transported up through the vascular network to the endothelial
cells that comprise the lining of the metarterioles, via inter-cellular channels such as gap
junctions. With this communication mechanism, there would be no problem associated
with movement against the blood flow direction. Once these compounds have made it to
the metarteriole location, they can communicate with the precapillary sphincters to induce
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