Nakajima Y, Moriwaki G, Ikeda K, Fujise Y
Department of Anesthesiology and Intensive Care, Hamamatsu University School of Medicine, Japan.
Anesth Analg. 1997 Sep;85(3):593-9. doi: 10.1097/00000539-199709000-00020.
Isoflurane is an appropriate anesthetic for neuroanesthesia. We evaluated whether the effect of sevoflurane is similar to that of isoflurane or halothane on brain energy metabolism after cerebral ischemia followed by reperfusion using 31P-magnetic resonance spectroscopy. Wistar rats (n = 21) were divided into three groups: isoflurane-, sevoflurane-, or halothane-treated. After anesthesia induction and surgical preparation, each anesthetic concentration was adjusted to 1 minimum alveolar anesthetic concentration. Cerebral ischemia was induced with bilateral carotid occlusion and reduction of mean arterial blood pressure to 30-40 mm Hg by blood withdrawal. Magnetic resonance measurements were performed during ischemia and for 120 min of reperfusion. Intracellular pH in the isoflurane-treated, sevoflurane-treated, and halothane-treated groups decreased to 6.180 +/- 0.149, 6.125 +/- 0.134, and 6.027 +/- 0.157, respectively, at the end of ischemia. There were no differences in the change of phosphorous compounds and intracellular pH between the isoflurane-treated and the sevoflurane-treated groups during ischemia and reperfusion. However, in the halothane-treated group, we observed a significant delay in the recovery of adenosine triphosphate and intracellular pH (0.038 +/- 0.013 pH unit/min compared with 0.064 +/- 0.011 in the isoflurane-treated group and 0.058 +/- 0.008 in the sevoflurane-treated group) until 24 min of reperfusion (P < 0.05). We conclude that sevoflurane has effects similar to isoflurane on brain energy metabolism during and after cerebral ischemia.
It is important to know whether anesthetics adversely effect brain metabolism during ischemia and reperfusion. A new anesthetic, sevoflurane, affected the brain in a manner similar to isoflurane, which has been used for many years as an anesthetic.
异氟烷是神经麻醉的一种合适麻醉剂。我们使用31P磁共振波谱法评估了七氟烷在脑缺血再灌注后对脑能量代谢的影响是否与异氟烷或氟烷相似。将21只Wistar大鼠分为三组：异氟烷处理组、七氟烷处理组或氟烷处理组。诱导麻醉并完成手术准备后，将每种麻醉剂浓度调整至1个最低肺泡有效浓度。通过双侧颈动脉闭塞并放血使平均动脉血压降至30 - 40 mmHg来诱导脑缺血。在缺血期间及再灌注120分钟内进行磁共振测量。在缺血结束时，异氟烷处理组、七氟烷处理组和氟烷处理组的细胞内pH分别降至6.180±0.149、6.125±0.134和6.027±0.157。在缺血和再灌注期间，异氟烷处理组和七氟烷处理组之间的磷化合物变化和细胞内pH没有差异。然而，在氟烷处理组中，我们观察到三磷酸腺苷和细胞内pH的恢复明显延迟（再灌注至24分钟时，氟烷处理组为0.038±0.013 pH单位/分钟，而异氟烷处理组为0.064±0.011，七氟烷处理组为0.058±0.008）（P < 0.05）。我们得出结论，七氟烷在脑缺血期间及之后对脑能量代谢的影响与异氟烷相似。
了解麻醉剂在缺血和再灌注期间是否对脑代谢产生不利影响很重要。一种新型麻醉剂七氟烷对脑的影响方式与已使用多年的麻醉剂异氟烷相似。
