Intracellular redox states under halothane and barbiturate anesthesia in normal, ischemic, and anoxic monkey brain.
Cortical reflectance, mean arterial blood pressuees, electroencephalograms, and cortical blood flow were continuously recorded together with fluorescence of reduced pyridine nucleotides (PN) at various carbon dioxide tensions before, during, and following middle cerebral artery occlusion in 10 squirrel monkeys receiving halothane or babiturate anesthesia. Measurements were continued through a nitrogen breathing cycle and to death produced by anoxia. The anesthetic agent produced no detectable differences in PN fluorescence in cerebral tissue during ischemia and anoxia. The known cerebral protective action of barbiturates is apparently unrelated to the intracellular redox state.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D002545:Brain Ischemia / Q000378:metabolism*; D002245:Carbon Dioxide / Q000378:metabolism; D002560:Cerebrovascular Circulation; D006221:Halothane / Q000494:pharmacology*; D000882:Haplorhini; D002534:Hypoxia, Brain / Q000378:metabolism*; D009243:NAD / Q000378:metabolism; D009249:NADP / Q000378:metabolism; D010084:Oxidation-Reduction / Q000187:drug effects; D010424:Pentobarbital / Q000494:pharmacology*; D013997:Time Factors
D009243:NAD; D002245:Carbon Dioxide; D009249:NADP; D010424:Pentobarbital; D006221:Halothane