AJP - Heart and Circulatory Physiology, Vol 243, Issue 2 181-H186, Copyright © 1982 by American Physiological Society
Reactive and exercise hyperemia during high levels of adenosine infusion
R. L. Hester, A. C. Guyton and B. J. Barber
In these experiments we tested the quantitative importance of adenosine as
a mediator in the regulation of muscle with blood containing adenosine at
concentrations more than 1,000 times the normal resting adenosine level (1,
7) so that the effect of any endogenously released adenosine would be
miniscule in comparison with the effect of this perfused adenosine.
Therefore, any major blood flow responses that should occur while the
muscle remained continuously under the influence of the perfused adenosine
could hardly be ascribed to endogenous adenosine. At the onset of the
perfusion with the adenosine the blood flow increased approximately
sevenfold. However, over 1-3 h of continued perfusion, the blood flow
returned to or near to control despite the extreme amounts of adenosine.
Then, while the muscle was still exposed to the adenosine, both reactive
hyperemia and exercise hyperemia were elicited for varying time periods and
varying degrees for a total of 96 separate measurements in 12 preparations.
In all instances the increases in blood flow during hyperemia were almost
exactly identical to those recorded prior to adenosine perfusion. Because
it would have been almost impossible for the small amounts of endogenous
adenosine to cause the large hyperemia responses in the face of the extreme
amounts of perfused adenosine, it is concluded that both the reactive and
exercise hyperemia responses are probably caused either entirely or almost
entirely by factors other than adenosine.
