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本实验成功地进行了人心肌肌球蛋白同工酶聚丙酰胺凝胶电泳分析。首次比较了不同年龄的人心肌肌球蛋白同工酶酶谱的差异,儿童心肌以V_1为主,成人以V_3为主。证实了前人根据动物实验提出的假说。同时对克山病患儿的心肌肌球蛋白同工酶进行了分析,证明克山病患者心肌由于坏死、崩解及“变性”使完整的无变化的肌球蛋白分子明显减少,认为这是造成心肌收缩力下降的主要原因。同时证明:克山病患儿心肌中残留的肌球蛋白同工酶向着省能的V_3为主的成人型变化。作者提出:这是对能量供应不足的一种代偿。但是,这种代偿能力较动物弱得多。本文最后探讨了防治克山病的一种可能途径。
This experiment successfully conducted human myocardial myosin isoenzyme polyacrylamide gel electrophoresis analysis. For the first time, the differences of myocardial myosin isoenzymes of different age groups were compared. V_1 was predominant in children and V_3 was the predominant in adults. Confirmed the previous hypothesis based on animal experiments. Myocardial myosin isoenzyme in children with Keshan disease was analyzed at the same time, which proved that the myocardium of Keshan disease was significantly reduced due to necrosis, disintegration and “degeneration”, which is considered as Cause the main reason for the decline of myocardial contractility. At the same time, it is proved that residual myocardial myosin isoenzyme in children with Keshan disease changes to adult-oriented V_3. The author puts forward: This is a kind of compensation for the insufficiency of energy supply. However, this compensatory capacity is much weaker than that of animals. Finally, this article explores a possible way to prevent Keshan disease.