Cerebral metabolic effects of naloxone administered with anesthetic and subanesthetic concentrations of halothane in the dog.

An abrupt significant increase in cerebral oxygen consumption when narcotic anesthesis is reversed by a narcotic antagonist has been reported. Since naloxone has also been reported partially to reverse nonnarcotic anesthesia, a similar effect might be expected were maloxone admininistered during exposure to inhalational anesthetics. To determine whether such a cerebral response should occur, naloxone, 1 and 10 mg/kg, was administered to eight dogs receiving an anesthetic concentration of halothane (0.87 per cent) or a subanesthetic concentration (0.3 per cent). Both naloxone doses failed to alter cerebral oxygen consumption at either halothane concentration. A transient EEG "reversal" was observed only after naloxone, 10 mg/kg, in animals breathing halothane, 0.87 per cent. These results would argue against any appreciable reversal of halothane anesthesia by naloxone. A significant increase in mean arterial blood pressure of 12 to 16 per cent followed naloxone administration at each condition. This is consistent with a previous report that interaction with specific receptors near the cardiovascular control center is responsible for this effect of naloxone.