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作 者:陈英茂[1] 刘自厚 张晓红[1] 高晓燕 周晓霞[2] 侯瑞田[2]
机构地区:[1]承德医学院低温生理研究室 [2]承德医学院生物化学教研室
出 处:《承德医学院学报》1991年第2期71-76,共6页Journal of Chengde Medical University
摘 要: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。The role of Ca^(2+) channel and Na^+-Ca^(2+) exchange in myocardial intracellular Ca^(2+)-overload was studied with the isolated working rat heart perfusion model. In all experimental groups, the content of protein in the outflow from coronary reperfused for 5 min after 25 min of global ischemia did not change significantly when compared with that of pre-ischemia. Theresults suggested that there was no myocardial sarco plasmic memorane dama geduring ischemia-reperfusion However, compared with the normal group, (1)reperfusion with the K-H solution significantly increased the content of Ca^(2+) and Na^+ in myocardium and decreased K^+; (2)reperfusion with the K-H solution containing verapamil(0.1mmol/L)did not signifieantly change the content of Ca^(2+), Na^+ and K^+ in myocardium; (3)reperfusion with the K-H solution containing verapamil (0.1mmol/L) and Mn^(2+)(0.5mmol/L)significantly increase the content of Ca^(2+) in myocardium and did not significantly change Na^+ and K^+;(4)reperfusion with the K-H solution containing verapami 1(0.1mmol/L)and more Na^+(add 3 more mmol of NaCl to a liter of it) significantly decreased the content of Ca^(2+) in myoeardium and significantly increased Na^+. These results show that before myocardial sarco plasmic membrane damage the change of Calcium channel activity plays an important role in forming intracellular Ca^(2+)-overload and Na^+-Ca^(2+) exchange mechanism is conducive to modulating intracellular Ca^(2+)-overload.
关 键 词:钙超负荷 钙通道 Na+—Ca2+交换 缺血再灌注 心脏
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