脑缺血和再灌注时脑血流量、能量代谢和水份含量的改变

Changes in blood flow, energy metabolism and water content in gerbil brain following cerebral ischemia and postischemic reperfusion

通过沙鼠脑缺血和再灌注动物实验,获得如下结果:(1)沙鼠50分钟脑缺血后血流再灌注的初期表现为充血状态,再灌注60分钟后进入迟发性低灌注期,并持续到再灌注120分钟。(2)在缺血50分钟时,缺血脑组织ATP、葡萄糖基本耗竭,乳酸大量积聚。血流再灌注60分钟脑内能量代谢迅速恢复,而于再灌注120分钟时,恢复的能量代谢继发性恶化。(3)脑缺血后出现明显脑水肿,血流再灌注初期,充血反应加重原有脑水肿程度。再灌注60分钟时,脑水肿基本纠正,再灌注120分钟时,伴随能量代谢恶化重又出现脑水肿。(4)实验结果表明,迟发性低灌注与再灌注期继发性能量代谢恶化和脑水肿密切相关,因而纠正迟发性低灌注是治疗脑缺血的关键之一。

The experimental result of cerebral ischemia and postischemic reperfusion in gerbil showed: (1)The ischemic brain showed hyperperfusion (congestion period)after 10 minutes reperfusion following 50 minutes of ischemia, and then entered a delayed hypoperfusion period after 60 minutes reperfusion which was remained till the end of 120 minutes of reperfusion. (2)after 50minutes of ischemia the ATP and glucose contents in brain tissure were almost depleted and lactate accumulated greatly. The cerebral energy metabolic state recovered rapidly within 60 minutes of reperfusion, and showed secondary deterioration after 120 minutes of reperfusion. (3)Cerebral edema occurred after cerebral ischemia, and further developed at the beginning of reperfusion, however edema alleviated obviously after 60 minutes reperfusion, but worse again after 120 minutes reperfusion. (4)The result in the present study also showed that secondary deteriorations in energy metabolism and cerebral edema colsely correlated with the delayed hypoperfusion, hence, correction of delayed hypoperfusion might be the key point in the treatment of cerebral ischemia.