论文部分内容阅读
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TXB_2含量由19.31±7.61pg/mg增至33.77±6.38pg/mg(P<0.05),Ca~(2+)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,TXB_2含量继续增至37,01±8.37pg/mg(P<0.05),Ca~(2+)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TXA_2、Ca~(2+)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。
Local cerebral ischemia and re-irrigation flow models were replicated by clipping the middle cerebral artery of the cat and clamping the perfusion. After 5 hours of vascular occlusion, γCBF in the ischemic region decreased from 106±12 ml/100 g/min to 17±4 ml/100 g/min (P<0.01). The amplitude of SEP decreased and cerebral edema appeared. Morphological examination also showed ischemic injury. The content of TXB_2 in cortex tissue increased from 19.31±7.61pg/mg to 33.77±6.38pg/mg (P<0.05), and the Ca2+ content increased from 10.4±1.2umol/g to 16.5±0.9umol/g (P <0.01). After 2 hours of re-infusion, γCBF only restored to 63±7 ml/100 g/min (P<0.01), suggesting a delayed hypogastric ischemia syndrome after ischemia; SEP amplitude was slightly restored at the beginning and severely suppressed later. The edema was further aggravated, the TXB 2 content continued to increase to 37,01±8.37 pg/mg (P<0.05), the Ca 2+ content increased to 20.1±3.0 μmol/g (P<0.01). Electron microscopy revealed mitochondrial swelling. A floc appears, indicating the deposition of a calcium phosphate salt. These results suggest that increased TXA_2 and Ca 2+ influx have a role in cerebral ischemia, especially in the pathogenesis of ischemia-reperfusion injury.