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本文以结扎家兔冠状动脉左室支为心肌缺血模型,应用镧电子示踪技术,生物体视学定量分析等方法,观察了心肌缺血不同时间再灌注后细胞膜系及线粒体超微结构以及镧示踪所提示的线粒体的功能变化等特点。结果表明,在心肌缺血20分时,细胞膜通透性升高,镧粒子进入细胞,再灌注时更为严重,即出现再灌注损伤。此时镧粒子多集于肌浆管。随缺血时间延长(30—40分),变化愈趋严重,缺血40分后再灌注,镧粒子大量涌入线粒体。而缺血60分,特别是再灌注时,心肌细胞严重破坏,几乎无完整线粒体,其中亦很少有镧颗粒。说明在此情况下的再灌损伤已属不可逆性。膜通透性的变化是由外及里的,即先肌膜而后为细胞内膜。就线粒体来讲则是先外膜而后内膜。实验结果提出可逆性(早期)再灌注损伤期,及不可逆性再灌注损伤期(晚期)的概念。
In this paper, left ventricular branches of rabbit coronary artery ligation model of myocardial ischemia, the use of electron transport lanthanum technique, quantitative analysis of biological methods, observed myocardial ischemia at different times after reperfusion cell membrane and mitochondrial ultrastructure and Lanthanum tracer prompted the mitochondrial function changes and so on. The results showed that in myocardial ischemia 20 minutes, the cell membrane permeability increased, lanthanum particles into the cells, reperfusion more serious, that is, reperfusion injury. At this time, more lanthanum particles set in the sarcoplasmic reticulum. With the prolongation of ischemia time (30-40 minutes), the change became more and more severe. After ischemia for 40 minutes, reperfusion occurred. Lanthanum particles influx into mitochondria. Ischemia of 60 points, especially when reperfusion, myocardial cell damage, almost no complete mitochondria, of which there are few lanthanum particles. Reperfusion injury in this case is already irreversible. Changes in membrane permeability is from outside and inside, that is, after the first muscle and endometrial membrane. In terms of mitochondria is the first outer membrane and then the intima. The experimental results proposed the concept of reversible (early) reperfusion injury and irreversible reperfusion injury (late).