异氟烷不同时间干预对大鼠不同程度全脑缺血的保护作用及其神经递质机制的探讨

目的评价异氟烷3种干预方式的脑保护效能,为临床提供脑缺血保护依据。方法雄性SD大鼠随机分为假手术组、对照组、预处理组、保护组、复苏组,后4组按缺血时间再分为缺血10min、15min及20min3个亚组。建立清醒全脑缺血模型。观察清醒、缺血及再灌注后海马谷氨酸递质浓度及BIS改变,记录翻正反射恢复的时间及运动功能评分。记数海马CA1区锥体细胞数和TUNEL阳性细胞的百分率。结果保护组在缺血15min翻正反射恢复时间短于预处理组(P<0.05)。保护组缺血10min和15min期间谷氨酸浓度低于预处理组和复苏组(P<0.01)。全脑缺血10min及15min,保护组海马CA1区神经细胞计数高于预处理组及复苏组(P<0.05)。缺血10min及15min保护组的细胞凋亡率明显低于预处理组和复苏组(P<0.05)。结论异氟烷麻醉下的脑保护效应要好于预处理及复苏;异氟烷预处理与复苏的脑保护效应相同。

Protective efficiency and neurotransmitter mechanism of three methods of isoflurane intervention on various levels of global cerebral ischemic injury in rats

Objective To evaluate the neurotransmitter mechanism and protective efficiency of three methods of isoflurane intervention on global cerebral ischemia, and to seek an effective method to improve cerebral ischemia damage. Methods Adult male Sprague-Dawley rats were randomly divided into sham operation group, control groups, preconditioning groups, protective groups and resuscitation groups. The rats of the last four groups were further divided into 10, 15 and 20min ischemia subgroups. The model of global cerebral ischemia and reperfusion was reproduced in waking rats 2 days before ischemia. The microdialysis samples were collected and BIS was recorded after reperfusion. The recovery of right reflection was observed after ischemia and the motor function was observed. All viable and apoptotic neurons were counted and the percentage of apoptotic neurons was calculated. The results showed that glutamate concentration in the hippocampus of protective groups was significantly lower compared with preconditioning group and resuscitation group. Results With ischemia fasting 10 and 15min (P<0.01), and glutamate concentration in the hippocampus of resuscitation groups was significantly lower compared with preconditioning group 0-15min after ischemia (P<0.05).The recovery time of reverse reflection in the protective groups was shorter compared with preconditioning group after ischemia for 15 min (P<0.05). The viable neurons in the CA1 sector of the hippocampus of the protective groups were significantly higher compared with preconditioning group and resuscitation group after ischemia for 10 and 15 min (P<0.05). The apoptosis rates in the CA1 sector of the hippocampus of protective groups were significant lower than preconditioning group and resuscitation group after 10 and 15 min ischemia (P<0.05). Conclusions Isoflurane anesthesia could produce better improve global cerebral ischemia-reperfusion injury, but the protective effect of preconditioning and resuscitation appears to be similar.