[非那嗪对实验性心肌梗死心脏收缩活动能量供应的影响]
[Effect of nonachlazine on the energy provision for cardiac contractile activity in experimental myocardial infarct].
作者信息
Reznikov K M, Provotorova P P, Sidel'nikova V I
出版信息
Farmakol Toksikol. 1982 Sep-Oct;45(5):52-7.
Experiments on 107 rabbits and 76 white rats with the use of electrophysiological, biochemical and electron microscopy research methods have shown that nonachlazine-induced improvement of heart contractility in microfocal myocardial infarction occurs as a result of the shortening of the systolic and lengthening of the diastolic phases of the heart cycle. Nonachlazine improves the processes of oxidative phosphorylation in heart mitochondria in myocardial infarction, which is accompanied by inhibition of the activity of succinate dehydrogenase and transition of oxidation from succinate to NAD-dependent substrates.
运用电生理、生化及电子显微镜研究方法，对107只家兔和76只白鼠进行的实验表明，在微灶性心肌梗死中，非那嗪诱导的心脏收缩力改善是由于心动周期收缩期缩短和舒张期延长所致。非那嗪可改善心肌梗死时心脏线粒体的氧化磷酸化过程，这伴随着琥珀酸脱氢酶活性的抑制以及氧化从琥珀酸向NAD依赖底物的转变。
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