Effects of Acute Hypoxia on the Cerebral Blood Flow and Heart Rate in Carp, Cyprinus carpio

Cerebral blood flow with a laser Doppler f10wmetry and heart rate were examined in carp, each weighing approximately 500 g, immobilized with a muscle relaxant (d-tubocurarine chloride, 4 mg/kg) during 50-min hypoxia and subsequent 30~min normoxia at a water temperature of 23± l'C. Under mild hypoxia (water Po. of 100 and 75 mmHg), cerebral blood flow and heart rate remained constant relative to the normoxic values (water 1'02 of approximately 150 mmHg). At levels of water 1'02 below 25 mmHg, cerebral blood flow was significantly increased, while heart rate was significantly decreased. At water P02 of 50 mmHg, some carp individually examined showed a marked increa e in cerebral bloud flow without bradycardia. In addition, an intramuscular injection of atropine sulfate (1.2 mg/kg) caused the increase in cerebral blood flow without bradycardia in carp subjected to hypoxia (water 1'02 of 25 mmIIg). These findings suggest that the mechanisms involved in the cerebral circulatory regulation in response to hypoxia are different from those underlying the bradycardiac response, indicating a vagal reflex mediated through the muscarinic cholinoceptor on the heart, and that cerebral circulatory regulation begins to act before the bradycardiac response in a respiratory chain. In a preliminary study, we found that elevation of cerebral blood flow in response to hypoxia was completely abolished by an intramuscular injection of an a-adrenoceptor antagonist (phentolamine methanesulfonate, 2 mg/ kg) .