Abstract
We have investigated the role of adenosine, a purine nucleoside and potent vasodilator of cerebral pial vessels, during both acute (0-60 sec) and sustained (2-5 min) changes in cerebral perfusion pressure. Brain adenosine concentrations are rapidly increased within 5 sec of the onset of systemic hypotension and parallel, in a temporal fashion, the changes in pial vessel diameter and alterations in cerebral vascular resistance. During sustained hypotension, brain levels of adenosine are increased even within the autoregulatory range. These data are constant with the hypothesis that adenosine is an important metabolic factor in cerebral autoregulation.
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