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目的评价异丙酚对脑缺血再灌注期间沙土鼠缺血去极化的影响。方法雄性沙土鼠24只,体重60-75g,随机分为2组(n=12):对照组和异丙酚组。两组均吸入1％氟烷后气管插管,机械通气,对照组持续吸入1％氟烷,异丙酚组停止吸入氟烷,静脉输注异丙酚1.2mg·kg-1·min-1。股动脉、静脉切开置管,监测平均动脉压(MAP),输液。监测两侧海马CA1区脑皮层直流电位、局部脑血流(rCBF)及直肠温度。1h后,双侧颈总动脉阻断5min,再灌注30min停止吸入氟烷或输入异丙酚。结果缺血即刻两组MAP升高40％,rCBF几乎降至0,再灌注期逐渐恢复至缺血前水平;与对照组比较,异丙酚组脑缺血去极化的起始时间延长(P<0.01),持续时间及恢复时间差异无统计学意义(P> 0.05)。结论异丙酚可延长脑缺血再灌注期间沙土鼠缺血去极化起始时间,而对脑缺血去极化的持续时间及恢复时间无影响。
Objective To evaluate the effect of propofol on ischemia / depolarization in gerbils during cerebral ischemia / reperfusion. Methods 24 male gerbils weighing 60-75g were randomly divided into 2 groups (n = 12): control group and propofol group. After inhalation of 1% halothane, both groups were intubated and mechanically ventilated. In the control group, 1% halothane was inhaled continuously. In the propofol group, inhalation of halothane was stopped. Intravenous infusion of propofol 1.2 mg · kg -1 · min -1 . Femoral artery, vein catheterization, monitoring of mean arterial pressure (MAP), infusion. The cortical DC potential, regional cerebral blood flow (rCBF) and rectal temperature were measured in hippocampal CA1. After 1h, the bilateral common carotid artery was blocked for 5min, and then the inhalation of halothane or propofol was stopped 30min after reperfusion. Results Immediate ischemia in both groups increased MAP by 40%, rCBF almost dropped to 0, and gradually reverted to pre-ischemic level after reperfusion. Compared with the control group, the onset of cerebral ischemia and depolarization in propofol group was prolonged ( P <0.01). There was no significant difference between duration and recovery time (P> 0.05). Conclusion Propofol prolongs the onset time of ischemia and depolarization in gerbils during cerebral ischemia and reperfusion, but has no effect on the duration and recovery time of cerebral ischemia and depolarization.