Newberg L A, Michenfelder J D
Anesthesiology. 1983 Jul;59(1):29-35. doi: 10.1097/00000542-198307000-00006.
The cerebral metabolic effects of isoflurane suggest that it may provide a degree of cerebral protection similar to that demonstrated for barbiturates. Accordingly, the possible cerebral protection afforded by isoflurane against hypoxemia and ischemia was studied in mice and dogs, respectively. In mice breathing 5% oxygen survival time was increased significantly over control in groups exposed to 1.0% and 1.4% isoflurane. At higher concentrations (2.0% and 3.0%) it is presumed that cardiorespiratory depression contributed to shorter survival times. In six dogs the effects of 3% isoflurane on the rates of cerebral ATP and phosphocreatine depletion and lactate accumulation during incomplete global ischemia were compared with six control dogs exposed to N2O. Incomplete global ischemia was produced by acute hemorrhagic hypotension to 30 mmHg for 9 minutes, a situation that does not abolish cortical electrical activity (active EEG). In the dogs exposed to isoflurane, the cerebral energy stores of ATP and PCr and the cerebral energy charge were sustained at significantly higher levels than in dogs exposed to N2O, and the cerebral lactate accumulation was significantly less in the initial 7 minutes of hypotension. It is concluded that in the circumstances of oxygen deprivation insufficient to abolish cortical electrical activity, isoflurane, like the barbiturates, can provide some cerebral protection presumably by depressing cortical electrical activity and cerebral metabolism.
异氟烷对大脑代谢的影响表明，它可能提供一定程度的脑保护，类似于巴比妥类药物所显示的脑保护作用。因此，分别在小鼠和狗身上研究了异氟烷对低氧血症和局部缺血可能提供的脑保护作用。在吸入5%氧气的小鼠中，暴露于1.0%和1.4%异氟烷的组的存活时间比对照组显著延长。在更高浓度（2.0%和3.0%）下，推测心肺抑制导致存活时间缩短。将6只狗暴露于3%异氟烷下，观察其在不完全性全脑缺血期间脑ATP和磷酸肌酸消耗率以及乳酸积累情况，并与6只暴露于N2O的对照狗进行比较。通过急性出血性低血压使血压降至30 mmHg并持续9分钟来产生不完全性全脑缺血，这种情况不会消除皮层电活动（脑电图仍有活动）。暴露于异氟烷的狗，其脑内ATP和PCr的能量储备以及脑能量电荷维持在显著高于暴露于N2O的狗的水平，并且在低血压最初7分钟内脑乳酸积累明显较少。得出的结论是，在不足以消除皮层电活动的缺氧情况下，异氟烷与巴比妥类药物一样，可能通过抑制皮层电活动和脑代谢来提供一定的脑保护作用。
