EFFECTS OF DESFLURANE AND PROPOFOL ON ELECTROPHYSIOLOGICAL PARAMETERS DURING AND RECOVERY AFTER HYPOXIA IN RAT HIPPOCAMPAL SLICE CA1 PYRAMIDAL CELLS

被引:15
作者
Wang, J. [1 ]
Cottrell, J. E. [1 ]
Kass, I. S. [1 ,2 ,3 ]
机构
[1] Suny Downstate Med Ctr, Dept Anesthesiol, Brooklyn, NY 11203 USA
[2] Suny Downstate Med Ctr, Dept Physiol & Pharmacol, Brooklyn, NY 11203 USA
[3] Suny Downstate Med Ctr, Robert F Furchgott Ctr Neural & Behav Sci, Brooklyn, NY 11203 USA
关键词
volatile anesthetic; ischemia; neuronal damage; anoxia; hypoxic depolarization; hypoxic hyperpolarization; FOCAL CEREBRAL-ISCHEMIA; REDUCES INFARCT SIZE; SENSITIVE POTASSIUM CHANNELS; NEURONS IN-VITRO; M-ZETA SYNTHESIS; VOLATILE ANESTHETICS; BIOCHEMICAL-CHANGES; ARTERY OCCLUSION; BRAIN ISCHEMIA; ANOXIC DAMAGE;
D O I
10.1016/j.neuroscience.2009.02.027
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Cerebral ischemia is a major cause of death and disability and may be a complication of neurosurgery. Certain anesthetics may improve recovery after ischemia and hypoxia by altering electrophysiological changes during the insult. Intracellular recordings were made from CA1 pyramidal cells in hippocampal slices from adult rats. Desflurane or propofol was applied 10 min before and during 10 min of hypoxia (95% nitrogen, 5% carbon dioxide). None of the untreated CA1 pyramidal neurons, 46% of the 6% desflurane- and 38% of the 12% desflurane-treated neurons recovered their resting and action potentials 1 h after hypoxia (P<0.05). Desflurane (6% or 12%) enhanced the hypoxic hyperpolarization (4.9 or 4.7 vs. 2.6 mV), increased the time until the rapid depolarization (441 or 390 vs. 217 s) and reduced the level of depolarization at 10 min of hypoxia (-13.5 or -13.0 vs. -0.6 mV); these changes may be part of the mechanism of its protective effect. Either chelerythrine (5 mu M), a protein kinase C inhibitor, or glybenclamide (5 mu M), a K-ATP channel blocker, prevented the protective effect and the electrophysiological changes with 6% desflurane. Propofol (33 or 120 mu M) did not improve recovery (0 or 0% vs. 0%) 1 h after 10 min of hypoxia; it did not significantly enhance the hypoxic hyperpolarization (3.6 or 3.1 vs. 2.6 mV) or increase the latency of the rapid depolarization (282 or 257 vs. 217 s). The average depolarization at 10 m of hypoxia with 33 mu M propofol (-4.1 mV) was slightly but significantly different from that in untreated hypoxic tissue (-0.6 mV). Desflurane but not propofol improved recovery of the resting and action potentials in hippocampal slices after hypoxia, this improvement correlated with enhanced hyperpolarization and attenuated depolarization of the membrane potential during hypoxia. Our results demonstrate differential effects of anesthetics on electrophysiological changes during hypoxia. (C) 2009 IBRO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:140 / 148
页数:9
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