卡托普利对缺血－再灌注心肌的保护作用

Protection of reperfusion myocardial ischemia by captopril

在大鼠心脏Ｌａｎｇｅｎｄｏｒｆｆ灌流模型上观察缺血。再灌注（Ｉ／Ｒ）时心肌局部血管紧张素ＩＩ（ＡＧＴＩＩ）的变化及卡托普利（ｃａｐｔｏｐｒｉｌ）对心肌保护作用。缺血３０ｍｉｎ后再灌注，心肌ＡＧＴＩＩ含量升高６０％，钙含量增加１．８倍，蛋白漏出明显增多；肌浆网（ＳＲ）的摄钙量减少５５％。ｃａｐｔｏｐｒｉｌ能有效抑制ＡＧＴＩＩ的生成，减轻心肌细胞损伤，并明显改善ＳＲ的摄钙功能。１０－９ｍｏｌ／Ｌ的ＡＧＴＩＩ与正常ＳＲ温育，使ＳＲ的摄钙量降低４１％。这提示：Ｉ／Ｒ过程中，心肌局部ＡＧＴＩＩ生成增加是参与再灌注损伤的重要因素；而ＡＧＴＩＩ对ＳＲ钙转运功能的直接抑制可能是Ｉ／Ｒ后ＳＲ功能障碍的原因之一。

Abstract In the Langendorff perfusion model of rat heart,the changes of local angiotensin II(AG II) in myocardium and the myocardial protective effect of captopril during ischemia-reperfusion (I/R) were observed. During reperfusion after 30 min ischemia, myocardial AG II content increased 60% , calcium content increased 1. 8 fold, intracellular LDH and protein release increased significantly, and sarcoplasmic reticulum (SR) calcium uptake decreased 55%. Captopril inhibited effectively the production of AG II alleviated myocardial cellular injury, improved SR calcium up take significantly. After 10-9mol/L of AG II incubated with normal SR , calcium uptake decreased 41%. These results showed that the increased synthesis of myocardial AG II is responsible for the myocardium injury during I/R. Direct inhibitory effect of AG II on SR calcium transport may be one of the causes for the disturbance of SR function after reperfusion.