Patel P M, Drummond J C, Cole D J, Goskowicz R L
Department of Anesthesiology, University of California, San Diego, USA.
Anesthesiology. 1995 Apr;82(4):996-1003. doi: 10.1097/00000542-199504000-00024.
The release of excitatory neurotransmitters during ischemia is thought to contribute to ischemic neuronal injury. Volatile anesthetics have been shown to reduce excitatory neurotransmission in vitro, and it is conceivable that they reduce ischemia-induced neurotransmitter release. The current investigation was conducted to evaluate the effect of isoflurane and N2O-fentanyl anesthesia on ischemia-induced glutamate release in the rat and to compare it with that of mild hypothermia, an intervention known to reduce glutamate release significantly.
Microdialysis probes were implanted into the parietal cortex and dorsal hippocampus of four groups of anesthetized rats (n = 5 per group). The hypothermic group was anesthetized with 1.2% halothane. The two isoflurane groups were anesthetized with 0.5 minimum alveolar concentration or electroencephalographic burst-suppression doses of isoflurane (approximately 2 minimum alveolar concentration). The control group was anesthetized with 70% N2O-30% O2 and fentanyl. The pericranial temperature was maintained at 34 degrees C in the hypothermic group and at 38 degrees C in the remaining groups. Ischemia was induced by bilateral carotid artery occlusion with simultaneous hypotension to 35 mmHg for 10 min, followed by a reperfusion period of 70 min. Dialysate was collected before, during, and after ischemia. The concentrations of glutamate and glycine in the dialysate were measured by high-performance liquid chromatography.
Preischemic glutamate and glycine concentrations in the dialysate were similar among the groups. Ischemia resulted in a significant increase in glutamate and glycine concentrations in the N2O-fentanyl groups in the parietal cortex and in the hippocampus. This increase in neurotransmitter concentrations did not occur in the hypothermic group in either structure. Isoflurane reduced glutamate concentrations in both structures and glycine concentrations in the hippocampus. In the parietal cortex, glycine concentrations did not increase in either isoflurane group.
Hypothermia inhibits ischemia-induced excitatory neurotransmitter release in the rat. Isoflurane, in comparison with a N2O-fentanyl-anesthetized state, significantly attenuates excitatory neurotransmitter release in the hippocampus. This effect of isoflurane is comparable to that of mild hypothermia.
缺血期间兴奋性神经递质的释放被认为会导致缺血性神经元损伤。挥发性麻醉剂已被证明在体外可减少兴奋性神经传递，因此可以设想它们能减少缺血诱导的神经递质释放。本研究旨在评估异氟烷和氧化亚氮 - 芬太尼麻醉对大鼠缺血诱导的谷氨酸释放的影响，并将其与轻度低温（一种已知能显著减少谷氨酸释放的干预措施）的影响进行比较。
将微透析探针植入四组麻醉大鼠（每组n = 5）的顶叶皮质和背侧海马体。低温组用1.2%氟烷麻醉。两个异氟烷组分别用0.5最低肺泡浓度或脑电图爆发抑制剂量的异氟烷（约2最低肺泡浓度）麻醉。对照组用70%氧化亚氮 - 30%氧气和芬太尼麻醉。低温组的颅周温度维持在34℃，其余组维持在38℃。通过双侧颈动脉闭塞并同时将血压降至35 mmHg持续10分钟诱导缺血，随后进行70分钟的再灌注期。在缺血前、缺血期间和缺血后收集透析液。通过高效液相色谱法测量透析液中谷氨酸和甘氨酸的浓度。
各组透析液中缺血前谷氨酸和甘氨酸浓度相似。缺血导致顶叶皮质和海马体中氧化亚氮 - 芬太尼组的谷氨酸和甘氨酸浓度显著增加。在这两种结构中，低温组均未出现神经递质浓度的这种增加。异氟烷降低了两种结构中的谷氨酸浓度以及海马体中的甘氨酸浓度。在顶叶皮质中，两个异氟烷组的甘氨酸浓度均未增加。
低温可抑制大鼠缺血诱导的兴奋性神经递质释放。与氧化亚氮 - 芬太尼麻醉状态相比，异氟烷可显著减弱海马体中兴奋性神经递质的释放。异氟烷的这种作用与轻度低温的作用相当。
