Artru A A, Steen P A, Michenfelder J D
Anesthesiology. 1980 Mar;52(3):217-20. doi: 10.1097/00000542-198003000-00005.
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.
据报道，当用麻醉拮抗剂逆转麻醉时，脑氧耗量会突然显著增加。由于也有报道称纳洛酮可部分逆转非麻醉性麻醉，因此在吸入麻醉剂期间给予马洛酮可能会有类似效果。为了确定是否会出现这种脑反应，对八只接受氟烷麻醉浓度（0.87%）或亚麻醉浓度（0.3%）的狗给予了1毫克/千克和10毫克/千克的纳洛酮。在两种氟烷浓度下，两种剂量的纳洛酮均未能改变脑氧耗量。仅在呼吸0.87%氟烷的动物中给予10毫克/千克纳洛酮后，观察到短暂的脑电图“逆转”。这些结果表明纳洛酮不会对氟烷麻醉产生明显的逆转作用。在每种情况下，纳洛酮给药后平均动脉血压显著升高12%至16%。这与之前的一份报告一致，即与心血管控制中心附近的特定受体相互作用是纳洛酮产生这种作用的原因。
