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本文用离体Langendorff灌流大鼠心脏造成急性心肌缺血 /再灌注损伤模型 ,观察间歇性低氧暴露保护心肌线粒体的作用。以聚合酶链式反应 (PCR)方法和电子显微镜技术 ,观察线粒体DNA (mtDNA4 834 )片段缺失和超微结构的变化。大鼠暴露于模拟海拔 5 0 0 0米低氧环境 (6h/d ,2 8d)明显降低mtDNA4 834 缺失的发生率 (2 8 5 7% ,vs常氧对照组 87 5 %P <0 0 5 ) ;而且能够明显减轻因缺血 /再灌注引起的心肌线粒体肿胀、线粒体嵴断裂、消失 ;较好地维持了线粒体的正常结构和形态。结果表明 ,间歇性低氧暴露能有效防止缺血 /再灌注引起的心肌线粒体损伤和mtDNA的片段缺失 ,此作用可能是间歇性低氧心肌保护作用的机制之一。
In this study, acute myocardial ischemia / reperfusion injury was induced by perfused rat heart with Langendorff in vitro and the effect of intermittent hypoxia exposure on myocardial mitochondria was observed. The changes of mitochondrial DNA (mtDNA4 834) fragment deletion and ultrastructure were observed by polymerase chain reaction (PCR) and electron microscopy. Exposure of rats to simulated hypoxia at a height of 500 m (6 h / d, 28 d) significantly reduced the incidence of mtDNA4 834 deletion (28.5% vs 87.5%, P <0.05 for normoxia control group ), But also mitigated the mitochondrial swelling and mitochondrial cristae that disappeared due to ischemia / reperfusion and maintained the mitochondrial normal structure and morphology. The results showed that intermittent hypoxia exposure can effectively prevent myocardial mitochondrial damage and mtDNA fragment deletion caused by ischemia / reperfusion, which may be one of the mechanisms of intermittent hypoxic myocardial protection.