摘要
用Ｌａｎｇｅｎｄｏｒｆｆ无做功非循环式离休心脏灌注模型，琥珀酸为呼吸链底物，分别以Ｒｈ１２３荧光染料流动透析法和荧光素一荧光素酶系统发光法来检测缺血／再灌注对心肌线粒体和内膜体跨膜电位及ＡＴＰａｓｅ合成活力的影响，并观察了丹参素的保护作用。结果发现：缺血２０ｍｉｎ，心肌线粒体能化前跨膜电位升高，能化态跨膜电位不变，再灌注２０ｍｉｎ后，线粒体能化前跨膜电位不变，能化态跨膜电位降低。去除线粒体外膜的内膜体，缺血时能化前跨膜电位升高的现象消失，其它各多数变化趋势与线粒体相同，说明缺血／再灌早期线粒体跨膜电位的变化与其外膜有关。内膜体ＡＴＰａｓｅ合成活力缺血时无变化，再灌时降低，与内膜体能化态跨膜电位变化相同。缺血组能化前内膜体体积缩小；丹参素对线粒体跨膜电位、内膜体跨膜电位和ＡＴＰ合成反应活性有明显的保护与恢复作用。
Changes of the transmembrane potential and the ATPase synthetic activity inmyocardial mitochondria and mitoplast during ischemia and reperfusion were studied in the isolatedLangendorff perfusion rat hearts. During early stage of ischemia(20min),the transmembrane poten-tial of mitochondria in the absence of succinate (NE) is increaced,but it was not significantly,changed in the presence of succinate(E).After reperfusion for 20 min,the transmemblane potentialin NE of mitochondria was not significantiy changed,it decreased in the E state. In the case ofmitoplast,the potential in both NE and E of ischemia was not changed.The potential change ofmitoplast was similar to that of mitochondria in reperfusion. The ATPase synthetic activity inischemia was not significantly changed although it was decreased in reperfusion. The volume ofmitoplast in NE reduced in ischemia. DS-182(salvianic acid)is very effective in recoveringtransmembrane potential,ATPase synthetic activity and volume of mitochondria and mitopiast.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1996年第2期190-193,共4页
Chinese Journal of Pathophysiology
