Involvement of adenosine in cerebral hypoxic hyperemia in the dog.
Theophylline, a competitive adenosine antagonist, was used to evaluate the role of adenosine in cerebral hypoxic hyperemia. Cerebral venous outflow was measured by the Rapela-Green technique in mongrel dogs anesthetized with pentobarbital sodium and ventilated artificially. Theophylline was infused locally into the cerebral arterial system during moderate [cerebral venous O2 tension (PO2) 27-29 mmHg] or severe (cerebral venous PO2 = 10-15 mmHg) hypoxia; theophylline had no direct vascular effects at the concentration used. Cerebral hyperemia was completely reversed during moderate hypoxia, but only partially reversed during severe hypoxia when theophylline was infused during maintained hypoxia. Theophylline had no effect on cerebral; perfusion pressure, blood flow, or vascular resistance during normoxia. In another group, theophylline had no effect on the cerebral hyperemia induced by hypercapnia. In separate experiments, local cerebral arterial infusion of adenosine or AMP during normoxia had no effect on cerebral hemodynamics at any infusion rate tested (up to 100 micrograms/min). This study supports the hypothesis that adenosine is involved in the hyperemia associated with cerebral hypoxia. However, the degree of involvement may be dependent on the degree of hypoxia.
D000241:Adenosine / Q000494:pharmacology / Q000502:physiology*; D000249:Adenosine Monophosphate / Q000494:pharmacology; D000818:Animals; D001783:Blood Flow Velocity; D001794:Blood Pressure / Q000187:drug effects; D002339:Carotid Arteries; D004285:Dogs; D005260:Female; D006935:Hypercapnia / Q000503:physiopathology; D006940:Hyperemia / Q000503:physiopathology*; D002534:Hypoxia, Brain / Q000503:physiopathology*; D007261:Infusions, Intra-Arterial; D008297:Male; D014655:Vascular Resistance / Q000187:drug effects
D000249:Adenosine Monophosphate; D000241:Adenosine