Newberg L A, Milde J H, Michenfelder J D
Anesthesiology. 1983 Jul;59(1):23-8. doi: 10.1097/00000542-198307000-00005.
The effects of 1.4-6.0% end-expired isoflurane on cerebral metabolism and hemodynamics were examined in dogs. A dose-related decrease in cerebral oxygen consumption (CMRO2) occurred until there was suppression of cortical electrical activity as reflected by the onset of an isoelectric electroencephalogram. This occurred at an end-expired concentration of 3% isoflurane when the mean CMRO2 was 2.02 ml X 100 g-1 X min-1. Thereafter, increasing concentrations of isoflurane to 6% had no further effect on the CMRO2. Brain biopsies taken at the end of the study revealed normal concentrations of ATP and phosphocreatine and a normal energy charge. Despite a normal cerebral energy state, there was a mild, dose-related, cerebral lactic acidosis (up to 2.84 mumol/g) that accompanied a mild systemic acidosis. It is concluded that the cerebral metabolic changes produced by isoflurane are secondary to an effect on cortical electrical activity, that abolition of this activity can be produced in dogs by a clinically relevant concentration of isoflurane (3%) without marked systemic hemodynamic effects, and that concentrations of isoflurane necessary to abolish cortical activity have no direct toxic effect on cerebral metabolic pathways.
研究了1.4 - 6.0%呼气末异氟烷对犬脑代谢和血流动力学的影响。脑氧耗量（CMRO2）呈剂量相关性下降，直至皮层电活动受到抑制，表现为等电位脑电图的出现。当呼气末异氟烷浓度为3%时出现这种情况，此时平均CMRO2为2.02 ml×100 g-1×min-1。此后，将异氟烷浓度增至6%对CMRO2不再有进一步影响。研究结束时采集的脑活检显示ATP和磷酸肌酸浓度正常，能量电荷正常。尽管脑能量状态正常，但伴有轻度全身酸中毒的同时，存在轻度、剂量相关性的脑乳酸酸中毒（高达2.84 μmol/g）。得出的结论是，异氟烷引起的脑代谢变化继发于对皮层电活动的影响，临床相关浓度的异氟烷（3%）可在犬体内消除这种活动，且无明显全身血流动力学影响，消除皮层活动所需的异氟烷浓度对脑代谢途径无直接毒性作用。
