Respiratory Responses to Common Carotid Occlusion in the Rat: Evidence for Involvement of Adenosine

Abstract

It is well established that ischemic/hypoxic situations increase the levels of endogenous adenosine. At the heart, during myocaridal ischemia, the rat coronary venous overflow of adenosine increases markedly (Richardt et al., 1987). In the dog, with as little as 5 s of ischemia, myocardial adenosine levels increase almost three-fold (Berne, 1980). Also in the human heart the content of adenosine in the myocardium during conditions of ischemia/hypoxia increases enormously (Sollevi, 1986). At the brain, the extracellular concentrations of adenosine at the rat striatum during ischemia are greater than in basal conditions (Hagberg et al., 1987). Adenosine levels in the artificial cerebro spinal fluid perfusates of the rat cerebral cortex increase after inhalation of 5% O₂ (Phillis et al., 1988). Increase (from 0.96 ± 0.07 nmol/g to 2.3 ± 0.31 nmol/g) in adenosine levels is detected within 5 s after the onset of ischemia in rat brains (Winn et al., 1979). Within 30 s of the onset of hypoxia, brain adenosine levels in rats increase paralleling temporally the changes in cerebral blood flow (Winn et al., 1981). In other tissues; in kidney tissues and urine of both cats and rats, adenosine levels significantly increase after renal artery occlusion during 2 min (Miller et al., 1978); plasma adenosine concentrations in the human forearm vein increase during ischemic work (Sylvén et al., 1988).