摘要
通过建立兔心肌缺血预适应模型,观察缺血预适应时的心肌保护效应、乳酸代谢和冠状动脉(动脉)血管内皮细胞释放内皮素的变化。结果发现:缺血预适应可明显减少缺血和再灌注损伤后的梗塞面积(P<0.01),乳酸生成率降低(P<0.01),内皮素的释放量减少(P<0.05)。认为:缺血预适应可明显增加心肌细胞对缺血和再灌注性损伤的耐受力,其机理与心肌细胞代谢降低、乳酸生成率减少和冠脉血管内皮细胞释放内皮素量减少有关。
Abstract The myocardial ischemic-preconditioning(IP) rabbit model was estabolished to observe the protective effect of myocardium IP and its relation to the changes of myocardial lactate production and endothelin released from coronary endothelium. Resuts showed that myocardial IP could markedly reduce the infarct size induced by ischemic-reperfusion(IR) injury(P<0.01);and myocardial lactate extraction ratio is decreased(P<0.01), and coronary endothelin level is lowered(P<0.05) with myocardial IP. We conclude that myocardial IP may markedly improve the tolerence of myocardial cell to IR injury and this effest is related to the reduced myocardial lactate production and the decreased release of endothelin from coronary endothelium.
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
1995年第6期363-365,共3页
Journal of Clinical Cardiology