急性运动心肌缺氧对大鼠心肌纤维和线粒体膜结构及功能的影响

EFFECTS OF ACUTE EXERCISE INDUCED HYPOXIA ON MYOCARDIAL FIBERS AND STRUCTURE AND FUNCTION OF MYOCARDIAL MITOCHONDRIAL MEMBRANE IN RAT

采用递增负荷耗竭运动模型为急性缺氧应激源，观察了ＳＤ大鼠急性运动至力竭后心肌组织和线粒体膜过氧化脂质含量，线粒体内膜ＮＡＤＨ－ＣｏＱ还原酶活性变化和心肌纤维和线粒体超微结构。结果表明，心肌能量需求过高性缺氧应激后大鼠心肌组织匀浆和线粒体膜过氧化脂含量分别增高１４０．９％和３９．４％（Ｐ＜０．０１和Ｐ＜０．０５），线粒体内膜ＮＡＤＨ－ＣｏＱ还原酶活性降低６１．６％（Ｐ＜０．０５），心肌纤维和线粒体超微结构呈缺氧损伤性改变。研究提示。

The present study investigates lipid peroxide contents of myocardial tissue and mitochondrial membrane, the NADH CoQ reductase activity of inner mitochondrial membrane and the ultrastructure of myocardial fibers and mitochondria in SD rat after acute exercises to exhaustion adopting an incremental exhaustied exercise model as acute hypoxia stress source. Results show that lipid peroxide contents of myocardium and myocardial mitochondrial membrane increase by 140.9% and 39.4% respectively (P<0.01 and P<0.05), the NADH CoQ reductase activity of inner mitochondrial membrane decreases by 61.1% (P<0.05) and ultrastructures of myocardial fibers and mitochondria present hypoxic pathological changes in rat with high energy demand myocardium after the hypoxia stress. The research suggests that the lipid peroxidation may be responsible for structural changes of myocardium and myocardial mitochondrial membrane during acute exercise induced hypoxia stress.