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Coupling of the Functional Stability of Rat Myocardium and Activity of Lipid Peroxidation in Combined Development of Postinfarction Remodeling and Diabetes Mellitus

机译:梗死后重塑与糖尿病合并发展中大鼠心肌功能稳定性与脂质过氧化活性的耦合

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摘要

Coupling of the functional stability of rat myocardium and activity of lipid peroxidation processes in combined development of postinfarction remodeling and diabetes mellitus has been studied. The functional stability of myocardium was studied by means of the analysis of inotropic reaction on extrasystolic stimulus, the degree of left ventricular hypertrophy, and the size of scar zone. It was shown that in combined development of postinfarction cardiac remodeling of heart (PICR) with diabetes mellitus (DM) animal body weight decreased in less degree than in diabetic rats. Animals with combined pathology had no heart hypertrophy. The amplitude of extrasystolic contractions in rats with PICR combined with DM had no differences compared to the control group. In myocardium of rats with PICR combined with DM postextrasystolic potentiation was observed in contrast with the rats with PICR alone. The rats with combined pathology had the decreased value of TBA-active products. Thus, the results of study showed that induction of DM on the stage of the development of postinfarction remodeling increases adaptive ability of myocardium. It is manifested in inhibition of increase of LPO processes activity and maintaining of force-interval reactions of myocardium connected with calcium transport systems of sarcoplasmic reticulum of cardiomyocytes.
机译:研究了大鼠心肌功能稳定性与脂质过氧化过程活性在梗死后重塑和糖尿病联合发展中的耦合作用。通过对收缩前刺激的正性反应,左心室肥大程度和瘢痕区大小的分析,研究了心肌的功能稳定性。结果表明,在梗塞后心脏的重塑(PICR)与糖尿病(DM)的共同发展中,动物体重的减轻程度小于糖尿病大鼠。合并病理的动物没有心脏肥大。与对照组相比,PICR合并DM的大鼠收缩前收缩幅度没有差异。与单独使用PICR的大鼠相比,在PICR合并DM的大鼠心肌中观察到了收缩后收缩增强。合并病理的大鼠的TBA活性产物值降低。因此,研究结果表明,在梗死后重塑发展的阶段诱导DM提高了心肌的适应能力。它表现为抑制LPO过程活性的增加和维持与心肌细胞质浆网钙转运系统有关的心肌的力间隔反应。

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