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采用低压低灌流60分钟造成家兔急性不完全性脑缺血,然后除去双侧颈总动脉的结扎并输回放出的全部血液进行重灌流。检测了皮层脑电图、心输出量及平均动脉血压;于重灌流120分时,测定脑静脉血乳酸脱氢酶(LDH)及磷酸肌酸激酶(CPK)活性,处死动物测定大脑皮质水、钠、钾及环核苷酸含量,观察组织形态学改变。实验结果见重灌流期间脑电图先有所恢复后严重抑制、大脑皮质水肿程度加重,CAMP 含量进一步升高,脑静脉血 LDH 及 CPK 活性显著升高、组织形态学呈现明显的缺血性损伤尤以亚微结构的改变为重,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。
Acute incomplete cerebral ischemia in rabbits was induced by hypo-hypoperfusion and perfusion for 60 minutes. The bilateral common carotid arteries were removed and all the released blood was transfused for reperfusion. The cortical EEG, cardiac output and mean arterial pressure were measured. The cerebral venous blood lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) activity were measured at 120 minutes after perfusion. The animals were sacrificed to determine the cerebral cortex water, Sodium, potassium and cyclic nucleotide content, observe the histological changes. The results of the experiment showed that during the period of reperfusion, the EEG was severely inhibited after the recovery of the EEG. The degree of edema in the cerebral cortex was aggravated. The content of CAMP increased further. The activity of LDH and CPK in cerebral venous blood increased significantly, and the histopathology showed obvious ischemic injury In particular, changes in sub-microstructure as heavy, indicating that tissue damage after severe reperfusion perfusion. The author analyzes possible mechanisms for the above changes.