【摘要】 用夹闭猫一侧大脑中动脉和开夹重灌流的方法,复制局部脑缺血和重灌流动物模型。发现血管闭塞5小时后,缺血区γCBF由106±12ml/100g/min降至17±4ml/100g/min（P<0.01）,SEP幅度下降和出现脑水肿,形态学检查亦见缺血损伤,皮层组织TXB₂含量由19.31±7.61pg/mg增至33.77±6.38pg/mg（P<0.05）,Ca²⁺含量由10.4±1.2umol/g增至16.5±0.9umol/g（P<0.01）。重灌2小时后,γCBF仅恢复至63±7ml/100g/min（P<0.01）,提示出现缺血后延迟型低灌综合征;SEP幅度初期有轻微恢复,后又呈严重抑制状态,脑水肿进一步加重,TXB₂含量继续增至37,01±8.37pg/mg（P<0.05）,Ca²⁺含量增至20.1±3.0μmol/g（P<0.01）,电镜可见线粒体肿胀,基质出现絮状物,表明有磷酸钙盐沉积。这些结果说明TXA₂、Ca²⁺内流增加在脑缺血,特别是缺血重灌流损伤发病中有一定作用。更多还原

【Abstract】 The models of socal cerebral ischemia and reperfusion were produced in cats by clipping the middle cerebral artety and removing the clip. Tha results indicated that after 5 hrs of ischemia, the γCBF decreased from 106±12ml/100g/min to 17±4ml/ 100g/min （P<0.01）. The amplitude of SEP declined and the brain edema developed. Ischemia damage was demonstrated morphologically, and the content of TXB₂ increased from 19.31±7.61pg/mg to 33.77±6.38Pg/mg （P<0.05） and the one of calcium from 104±1.2μmol/g to 16.5±0.9μtmol/g （P<0.01） in the ipsilateral cerebral cortex. With 2 hrs of reperfuslon, the rCBF recovered only to 63±7ml/100g/min （P<0.01）, suggesting that the delayed postischemic hypopeffusion develop, and the amplitude of SEP rose slightly but then declined severely and the brain edema worsened. The content of TXB₂ increased further to 37.01±8.37Pg/mg（P<0.05） and the one one of calcium to 20.1±3.0 μmol/g（P<0.01）.The electromicroscopy demonstrated that mitochondria be swollen and contain large flucculent densities in the matrex, suggesting that they be calcium phosphate deposits. These results indicated that the increase of TXA₂ and calcium influx may play an important role in pathogenesis of cerebral ischemia, especially ischemic repeffusion injury.更多还原