Reactive and exercise hyperemia during high levels of adenosine infusion

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.