人参总皂甙抗心肌缺血-再灌注损伤的作用机制  

Study on the Mechanism of Ginsenosides Against Ischemia reperfusion Injury of Myocardium

作　　者：侯明晓[1] 敖定椿[2] 

机构地区：[1]沈阳军区总医院心血管外科,沈阳110015 [2]大连医科大学附属第一医院胸心外科

出　　处：《中国胸心血管外科临床杂志》2000年第4期256-259,共4页Chinese Journal of Clinical Thoracic and Cardiovascular Surgery

摘　　要：目的　探讨人参总皂甙抗心肌缺血 -再灌注损伤作用及其作用机制。　方法　成年杂种犬 16条随机分为两组 ,每组 8条。对照组 :分别于主动脉阻断前 1小时和再灌注即刻 2次静脉滴注生理盐水各 10 0 ml;用药组 :分别于相同时间 2次静脉滴注含人参总皂甙 (12 .5 mg/ kg)的生理盐水各 10 0 ml,通过常温体外循环动物模型 ,测定血流动力学、细胞内游离钙浓度、心肌细胞线粒体磷脂含量、线粒体钙泵活性和心肌组织化学等 ,研究人参总皂甙的心肌保护机制。　结果　再灌注 30分钟和 6 0分钟时人参总皂甙能明显改善再灌注期间心脏收缩和舒张功能 ,两组左心室收缩压、左心室压力变化率比较差异有显著性 (P<0 .0 1) ,用药组心肌细胞内游离钙浓度明显低于对照组 (P<0 .0 1) ,线粒体磷脂含量、线粒体钙泵活性高于对照组 (P<0 .0 1) ,用药组心脏再灌注后心律失常发生率明显低于对照组 (P<0 .0 1)。心肌组织化学检查表明用药组以 0级和 1级为主 ,对照组以 3级和 2级为主 ,两组比较差异有显著性 (P<0 .0 1)。结论　人参总皂甙抗心肌缺血 -再灌注损伤的作用机制除提供能量基质 ,增加底物水平磷酸化 ,促进三磷酸腺苷、磷酸肌酸合成外 ,主要是由于其保护心肌细胞线粒体钙泵活性 ,减少线粒体膜磷脂降解 ,保护膜系统完整 ;降低细?Objective To study the Ginsenosides against ischemia reperfusion injury of myocardium.\ Methods Sixteen dogs were randomly divided into two groups.Control group ( n =8) received 100ml of normal saline, Ginsenosides group( n =8) separately received 100ml of normal saline with Ginsenosides 12.5mg/kg before ischemia and the initial of reperfusion.Through the animal model of nomothermic extracorporeal circulation,we studied the effects of Ginsenosides on recovery of myocardial function,intracellular free calcium concentration,membrane phospholipids of mitochondria analysis,calcium magnesium adenosinetriphosphatase activities of mitochondria and histochemistry of myocardium\ Results\ Ginsenosides could significantly improve cardiac contractility and diastolic function after 30 minutes and 60 minutes of reperfusion. The comparison of left ventricular systolic pressure,rates of change of left ventricular pressure between the two groups were remarkable ( P <0.01). Also Ginsenosides could markedly reduce the level of intracellular free calcium concentration ( P <0.01),prevent the decrease of membrane phospholipids of mitochondria ( P <0.01),and preserve the activities of Ca 2+ Mg 2+ adenosinetriphosphatase of mitochondria ( P <0 01). Ginsenosides could also reduce the rate of happening arrhythemia during reperfusion ( P <0.01).The histochemical responses in Ginsenosides group was highly superior to those in the control group ( P <0 01). \ Conclusion\ Ginsenosides can prevent ischemia reperfusion injury.The major mechanisms of anti reperfusion injury are:(1) to preserve the activities of Ca 2+ Mg 2+ adenosinetriphosphatase and reduce the decrease of membrane phospholipids of mitochondria,and protect the structure of membrane system.(2) to decrease the level of intracellular free calcium concentration,avoid the overload of calcium.

关 键 词：人参总皂甙 再灌注损伤 心肌缺血 钙 

分 类 号：R285.5[医药卫生—中药学] R259.422[医药卫生—中医学]