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在离体大鼠心脏灌流模型上,缺血25分钟后再灌注5分钟,实验各组在再灌注5分钟时冠脉流出液中的蛋白含量与缺血前相比无显著性变化,表明细胞膜无缺损。但是,和正常组相比,(1)K-H液再灌注导致心脏钙、钠含量显著增加,钾含量显著下降;(2)再灌液中加入异搏定使心脏各离子含量恢复正常;(3)再灌液中同时加入异搏定和Mn~(2+),又出现钙含量显著增加;(4)再灌液中加入异搏定的同时增加Na~+含量,出现钙含量显著下降。结果表明,在细胞膜缺损前,钙通道是钙超负荷发生的主要途径。Na~+-Ca~(2+)交换的作用,有助于减弱钙的超负荷。
In the isolated rat heart perfusion model, ischemia 25 minutes after reperfusion for 5 minutes, each group in the experimental group at 5 minutes after reperfusion, coronary effluent protein content compared with pre-ischemia had no significant change, indicating that the cell membrane No defect. However, compared with the normal group, (1) KH solution reperfusion resulted in a significant increase of calcium and sodium content in the heart and a significant decrease of potassium content; (2) Verapamil was added into the reperfusion solution to normalize the content of each ion in the heart; (3) ) Reperfusion solution with the addition of verapamil and Mn 2+, and a significant increase in calcium content; (4) Reperfusion solution with verapamil while increasing Na ~ + content, the calcium content decreased significantly. The results show that calcium channel is the main pathway of calcium overload before the cell membrane defect. The role of Na ~ + -Ca ~ (2+) exchange, helps to reduce the calcium overload.