家兔急性不完全性脑缺血及重灌流的实验研究

采用低压低灌流方法造成家兔急性不完全性脑缺血60分钟,缺血后进行重灌流。检测了脑电图(EEG)、心输出量、平均动脉血压及脑静脉血乳酸脱氢酶(LDH)、磷酸肌酸激酶(CPK)活性以及大脑皮质水、钠、钾及环核苷酸含量,观察组织形态学改变。实验结果表明通过低压低灌流成功地复制了兔急性不完全性脑缺血模型。其特点为EEG严重抑制、大脑皮质水、钠含量升高、LDH及CPK活性显著升高。并见脑组织出现脑水肿改变。重灌流期间EEG先有所恢复后严重抑制,LDH及CPK活性仍显著升高。大脑皮质cAMP含量进一步升高,水肿程度加重。组织形态学呈现明显的缺血性损伤尤以亚微结构更为严重,表明重灌流后组织损伤加重。作者分析了上述改变发生的可能机制。

Studies on acute incomplete cerebral ischemic and reperfusion damages in rabbits

Severe incomplete cerebral ischemia was induced in 70 rabbits using bilateral carotid artery occIusion coupled with hemorragic hypotension. 60 minutes of ischemia was followed by 2 hours of reperfusion. The electroencephalographic activity, cardiac output and mean artery blood pressure were measured at regular intervals. The activities of lactic dehydrogenase(LDH) and creatine phosphokinase(CPK) in cerebral venous blood were measured before and after the insult. The contents of water, sodium, potassium and cyclic uncleotides were determined in cerebral cortex after 60 min of ischemia and 120 min of reperfusion respectively. The histological and ultrastructural alterations were observed. The results indicate that the acute incomplete cerebral ischemie model in the rabbit can be successfully established by hypotension plus hypoperfusion. Its characteristics are severe suppression of electroencephalographic activity, significant eIevation of LDH and CPK, an increase in the contents of water and sodium. Ischemic edema was demonstrated morphologically in cerebral cortex. During the reperfusion peroid, initially some recovery of the electroencephaiographic activity appeared but then severe suppression occurred; the severety of brain edema was exacerbated; the content of cAMP was increased further and the activities of LDH and CPK were still significantly elevated. Severe ischemic tissue damage in cerebral cortex were morphologically demonstrated, of which the ultrastructural alterations were more remarkable. These results suggested that the ischemic tissue damage might be aggravated on reperfusion. The possible mechanisms were discussed. The cerebral circulatory disturbance and parenchymal insult during reperfusion peroid might play an important role in developing the irreversible postischemic brain damage.