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目的 :探讨顿抑心肌局部 5 羟色胺 (5 HT) ,去甲肾上腺素 (NE)和血小板聚集率的变化及顿抑心肌超微结构改变。方法 :采用冠状动脉结扎法建立兔顿抑心肌模型。用硝酸镧灌注固定心肌的电镜技术观察顿抑心肌超微结构改变。结果 :缺血后心肌局部 5 HT ,NE稍有升高 ,再灌注后心肌局部 5 HT ,NE含量明显高于正常对照组差别显著。血小板聚集率再灌注后明显升高 ,与对照组相比差异显著。顿抑心肌局部线粒体明显肿胀 ,基质紊乱 ,线粒体内外均有镧颗粒沉积 ,随着再灌注时间延长线粒体肿胀减轻 ,胞膜及线粒体膜完整。结论 :单胺类神经介质 5 HT ,NE参与了顿抑心肌的发生 ,血小板聚集率增加及 5 HT、NE含量增加是导致心功能延迟恢复的重要因素。顿抑心肌超微结构呈可逆性通透性改变 ,维持细胞膜结构的完整是心肌可逆性损伤的关键
Objective: To investigate the changes of local 5-HT, NE and platelet aggregation rate and myocardial ultrastructure in patients with stunned myocardium. Methods: The coronary artery ligation was used to establish the rabbit model of myocardial infarction. Electron microscopy of immobilized myocardium with lanthanum nitrate was used to observe the ultrastructural changes of the stunned myocardium. Results: Local 5 HT and NE increased slightly after ischemia, and the contents of 5 HT and NE in myocardium after reperfusion were significantly higher than those in normal control group. Platelet aggregation rate was significantly increased after reperfusion, compared with the control group, significant difference. Stunned myocardium mitochondria obvious swelling, matrix disorders, both inside and outside the mitochondria deposition of lanthanum particles, with reperfusion time mitigation of mitochondrial swelling, membrane and mitochondrial membrane integrity. CONCLUSION: 5 HT and NE, a monoamine neurotransmitter, are involved in the development of stunned myocardium. The increase of platelet aggregation rate and the increase of 5 HT and NE levels are the important factors leading to delayed recovery of cardiac function. Stunned myocardial ultrastructure was reversible permeability changes to maintain the integrity of the cell membrane structure is the key to myocardial reversible injury