Captopril对缺血再灌心肌线粒体电子质子偶联和氧化磷酸化的影响

The effect of captopril on proton-electron coupling and oxidative phosphorylation of cardaic mitochondria during ischemia reperfusion

为研究ｃａｐｔｏｐｒｉｌ对缺血／再灌注心肌的保护机制，本实验用Ｌａｎｇｅｎｄｏｒｆｆ无作功非循环式离体心脏灌流模型，琥珀酸为底物，分别用氧电极法和铁氢化钾脉冲法检测缺血再灌注中ｃａｐｔｏｐｒｉｌ对心肌线粒体呼吸链复合体Ⅱ＋Ⅲ＋Ⅳ段氧化磷酸化和复合体Ⅱ＋Ⅲ段质子电子偶联的影响ｑ结果发现：缺血及再灌注时呼吸控制率（ＲＣＲ）、ＡＴＰ合成速度升高的现象在保护组不出现，说明ｃａｐｔｏｐｒｉｌ对心肌线粒体呼吸功能有保护作用，ｃａｐｔｏｐｒｉｌ对缺血时线粒体复合体Ⅱ＋Ⅲ质子泵出速度和电子传递速度升高有进一步的调节作用，使质子电子偶联更紧密，Ｈ＋／２ｅ－恢复至对照水平。再灌时质子泵出速度的降低可被ｃａｐｔｏｐｒｉｌ逆转。

The rat hearts were perfused in a none-recirculating Langendorff system to investigate the effect of captopril on oxidative phosphorylation of complexⅡ+Ⅲ+Ⅳ and proton-electron coupling of complexⅡ+Ⅲduring ischemia and reperfusion using oxygen electrode and K 3Fe(CN) 6pulse method with succinate as substrate.The results showed that RCR and ATP ase synthesis rate are increased during ischemia and reperfusion, captopril(1×10 -5 )reversed RCR and ATPase synthesis rate to the control levels,suggesting that captopril protected respiratory function significantly,regulated oxidative phosphorylation of mitochondria.The initial rate of proton(H +) ejection and electron transfer by mitochondria increased,and H +/2e - decreased at ischemia.After captopril was added,these parameters were returned to control levels.This showed that captopril further regulated the initial rate of proton ejection and election transfer so that proton and electron coupled closely.Captopril reversed decreasing initial rate of proton at reperfusion. These results support captopril scavenged free radicals and protected mitochondria membrance. Our past investigations demonstrated that the decrease of H + ejection rate was induced mainlyby the production of O 2 - and the leak of H + through the mitochondria membrane during reperfusion,indicating that captopril may have free radical scavenging and membrane protecting effects.