Cerebral oxygen consumption in the rat: pharmacological stimulation and suppression, role of catecholaminergic mechanisms.
The relationship between cerebral oxygen consumption (CMRO2), cerebral blood flow and arterial CO2 tension was investigated during anaesthesia induced by halothane, pentobarbital, ethanol and nitrous oxide. The results obtained by halothane, pentobarbital and ethanol indicate a relationship between central suppressants and CO2 in decreasing CMRO2. During nitrous oxide anaesthesia, CMRO2 increased with increasing CO2 tension, an effect which could be prevented by beta-adrenergic receptor blockade. This indicates a role of catecholaminergic mechanisms in CMRO2 regulation (as is the case during immobilization stress and ethanol withdrawal) perhaps as a protective measure providing increased energy supply in the central nervous system during conditions of endogenous or exogenous stress.
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D002560:Cerebrovascular Circulation / Q000187:drug effects; D000431:Ethanol / Q000494:pharmacology*; D006221:Halothane / Q000494:pharmacology*; D006935:Hypercapnia / Q000378:metabolism*; D008297:Male; D009609:Nitrous Oxide / Q000494:pharmacology; D010101:Oxygen Consumption / Q000187:drug effects*; D010424:Pentobarbital / Q000494:pharmacology*; D051381:Rats
D000319:Adrenergic beta-Antagonists; D000431:Ethanol; D010424:Pentobarbital; D009609:Nitrous Oxide; D006221:Halothane