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目的:观察病毒性心肌病患者外周血淋巴细胞线粒体增生及线粒体膜磷脂脱失程度,并分析该损伤与心功能状态的关系。方法:电镜细胞化学法定量观察83例病毒性心肌病患者(病毒性心肌炎50例,扩张型心肌病33例;NYHA心功能Ⅰ级者45例,Ⅱ级者9例,Ⅲ级者16例,Ⅳ级者13例)外周血淋巴细胞线粒体增生及线粒体膜磷脂脱失程度,并按心功能分级进行分析。23例健康献血员外周血淋巴细胞为正常对照组。结果:病毒性心肌病患者外周血淋巴细胞线粒体明显增生,线粒体总数及>10个线粒体淋巴细胞所占比例显著增加,<5个线粒体的淋巴细胞所占比例显著降低;膜磷脂定位正常的线粒体所占比率显著下降,而膜磷脂脱失线粒体所占比率显著升高;心功能Ⅰ级的病毒性心肌病患者外周血淋巴细胞线粒体增生和膜磷脂脱失的程度已显著高于正常对照组,且这些变化随着心功能损伤的加重更为明显。结论:线粒体膜磷脂损伤是病毒性心肌病发生发展的一个重要机制。
Objective: To observe the mitochondrial hyperplasia and mitochondrial membrane phosphatide loss in peripheral blood lymphocytes of patients with viral cardiomyopathy, and to analyze the relationship between the injury and cardiac function. Methods: Electron microscopy was used to quantify 83 patients with viral cardiomyopathy (viral myocarditis in 50 cases, dilated cardiomyopathy in 33 cases; NYHA cardiac function in 45 cases, grade Ⅱ in 9 cases, grade Ⅲ in 16 cases, Ⅳ grade 13 cases) peripheral blood lymphocytes mitochondrial hyperplasia and mitochondrial membrane phospholipid loss, and according to the classification of cardiac function analysis. Twenty - three healthy blood donors’ peripheral blood lymphocytes were normal control group. Results: The mitochondria of peripheral blood lymphocytes in patients with viral cardiomyopathy significantly proliferated, the total number of mitochondria and the proportion of> 10 mitochondrial lymphocytes increased significantly, the proportion of lymphocytes in <5 mitochondria decreased significantly, and mitochondria The proportion of mitochondria was significantly decreased; the degree of mitochondrial hyperplasia and the loss of membrane phospholipids of peripheral blood lymphocytes in patients with grade I cardiomyopathy were significantly higher than those in normal controls These changes with the deterioration of cardiac function more obvious. Conclusion: Mitochondrial membrane phospholipid damage is an important mechanism of the development of viral cardiomyopathy.