Abstract
To elucidate the mechanisms of CBF augmentation during hypoxemic hypoxia, we applied continuous monitoring of CBF and metabolism to examine the participation of prostacyclin, nitric oxide (NO), and/or adenosine in these mechanisms. Cats (n=32) were anesthetized and ventilated artificially. Cerebrovascular reactivity to hypoxia was assessed by changes in CBF, brain tissue oxygen and carbon dioxide tensions, and mean arterial blood pressure (ΔCBF, ΔBrPO2, ΔBrPCO2, and ΔMABP) during a 3-min inhalation of 10% O2+90% N2 before and after the intracarotid administration of (1) indomethacin (1mg/kg, a cyclooxygenase inhibitor, n=11), (2) L-NG-monomethyl-arginine (LNMMA, 1μmol/kg/min, an inhibitor of nitric oxide synthesis, n=11), and (3) caffeine (20mg/kg, an adenosine antagonist, n=10). BrPO2 decreased significantly in all groups during the produced hypoxemic hypoxia. CBF significantly increased in this state before the administration of indomethacin, LNMMA, or caffeine, whereas it contrastively did not significantly increase after the administration of indomethacin or caffeine. In addition, CBF significantly decreased under hypoxia during the administration of LNMMA. Taken together, these results suggest that prostacyclin (PGI2), nitric oxide (NO), and adenosine may jointly participate in CBF augmentation during hypoxia.
