The effects of sevoflurane on recovery of brain energy metabolism after cerebral ischemia in the rat: A comparison with isoflurane and halothane
The effects of sevoflurane on recovery of brain energy metabolism after cerebral ischemia in the rat: A comparison with isoflurane and halothane
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DOI：
10.1097/00000539-199709000-00020
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发表时间：
1997-09-01
影响因子：
5.7
通讯作者：
Fujise, Y
中科院分区：
文献类型：
--
作者：
Nakajima, Y;Moriwaki, G;Fujise, Y
异氟醚是一种适用于神经麻醉的麻醉剂。我们利用p -31磁共振波谱技术评估七氟醚对脑缺血再灌注后脑能量代谢的影响是否与异氟醚或氟烷相似。Wistar大鼠（n = 21）分为三组：异氟烷组、七氟烷组和氟烷组。麻醉诱导后；手术准备时，每种麻醉浓度调整为1个最小肺泡麻醉浓度。双侧颈动脉闭塞诱导脑缺血，取血使平均动脉血压降至30 ~ 40 mm Hg。在缺血和再灌注120分钟时进行磁共振测量。异氟醚组、七氟醚组和卤烷组缺血结束时细胞内pH值分别降至6.180 +/- 0.149、6.125 +/- 0.134和6.027 +/- 0.157。异氟醚处理组和七氟醚处理组缺血再灌注时细胞内磷化合物和pH值变化无差异。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（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），直到再灌注24分钟（P < 0.05）。我们得出结论，七氟醚对脑缺血期间和脑缺血后的能量代谢有类似于异氟醚的影响。意义：了解麻醉剂在缺血和再灌注时是否对脑代谢有不良影响是很重要的。一种新的麻醉剂，七氟醚，以类似于异氟醚的方式影响大脑，异氟醚已被用作麻醉剂多年。
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 P-31-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. Implications: 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.