异氟烷和七氟烷对缺血神经元c-fos蛋白表达的影响和保护作用

目的　了解吸入麻醉药异氟烷和七氟烷对脑缺血神经元c fos蛋白表达的影响和保护作用。方法　用苏木素 伊红 (HE)染色法检测大鼠脑缺血梗塞体积和海马结构CA1～CA4亚区神经元损伤程度。用免疫组化法检测海马结构c fos蛋白的表达。结果　缺血 1h再灌 72h异氟烷组和七氟烷组脑梗塞体积显著小于缺血组 ;海马CA3和CA4亚区神经损伤程度也显著小于缺血组。缺血 1h再灌 4h ,在海马齿回 ,CA4亚区c fos蛋白样免疫反应率 ,吸入麻醉药组明显低于未吸入组。结论　异氟烷和七氟烷对缺血神经元有一定的保护作用。它们对c fos蛋白表达的衰减作用可能与其拮抗NMDA受体性质有关

Effect of inhaled anesthetics, isoflurane and sevoflurane, on c-fosproteinexpression and protective in ischemic neuron

AIM To study effect of inhaled anesthetics, isoflurane and sevoflurane, on c fos protein expression and protective role in rat hisppocampal formation following brain ischemia. METHODS Cerebral ischemia was produced by occlusion of left middle cerebral artery and both common carotid arteries for 1h in rats. Rats were inhaled isoflurana and sevoflurane respectively, during the ischemia. Cerebral coronal sections (10μm) were stained with hematoxylin and eosin (HE). Infarct volume and histological damage as assessed from HE stained coronal brain slices. Expressions of c fos protein were detected by immunohistochemical method. The number of c fos protein like immunoreactivity (CFPLI) positive neuronal cells were counted. RESULTS Infarct volume was significantly reduced in isoflurane group and sevoflurane group as compared to the ischemic group. Ischemia led to a loss of many neurons in the CA1 sector of the hippocampus which was not modified by the inhaled anesthetics treatment. In the other hippocampal areas which were less severly damaged by ischemia reduced neuronal damage was found in some levels with the inhaled anesthetics treatment. Inhaled anesthetice significantly reduced number of CFPLI neurons in ventral blade of the dentate gyrus at 1h of MCA/CCAs occlusion with 4h of reperfusion. Most of the neurons in dentate gyrus and dentate hilar area cells showed intense nuclear staining 4 h after ischemia. C fos protein expression of ischemic groups showed more intense than inhaled anesthetic groups in hippocampal formation 4h after ischemia. CONCLUSION Isoflurane and sevoflurane have protective effect in ischemic neuron. In animals inhaled isoflurane or sevoflurane during ischemia there was marked attenuation of c fos protein induction 4 h after ischemia. This may relate to inhibition of NMDA receptor by isoflurane or sevoflurane.