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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。
Acute incomplete cerebral ischemia in rabbits was induced by low-pressure and low-perfusion methods for 60 minutes, and reperfusion was performed after ischemia. Electroencephalogram (EEG), cardiac output, mean arterial blood pressure, cerebral venous blood lactate dehydrogenase (LDH), phosphocreatine kinase (CPK) activity, and cerebral cortex water, sodium, potassium, and cyclic nucleotide content were measured. , Observe the change of histomorphology. The experimental results show that the rabbit model of acute incomplete cerebral ischemia was successfully reproduced by low pressure and low perfusion. It is characterized by severe EEG inhibition, increased cerebral cortical water and sodium content, and increased LDH and CPK activity. And see brain tissue changes in brain edema. During the re-perfusion period, EEG recovered first and then severely inhibited. The activity of LDH and CPK was still significantly increased. Cerebral cortical cAMP content further increased, the degree of edema increased. The histomorphology showed obvious ischemic injury, especially in the sub-microstructure, indicating that tissue damage was aggravated after reperfusion. The author analyzes the possible mechanisms for the above changes.