Kakurskiĭ L V, Beskrovnova N N, Kudrin A N, Kogan A Kh, Nikolov S M
Kardiologiia. 1976 Nov;16(11):31-7.
Myocardial infarction was induced in rats by ligating a coronary artery. During a week they received daily injections of 50 mg/kg of vitamin E intramuscularly or 30 mug/kg of sodium selenite subcutaneously, or else a combination of these preparations. The control animals received no injections. Stereometrically a statistically significant reduction of the infarcted zone was noted under the effect of selenium, this reduction being especially distinct during the ischaemic stage; the maturation of granulation tissue with an enhancement of the fibroblast reaction therein was accelerated. The muscle cells of the myocardium beyond the infarction zone displayed an increased activity of lactate dehydrogenase and a reduced activity of succinate dehydrogenase, intactness of the ultrastructure of the cell pattern, an enhancement of the signs of ultrastructural regeneration. Vitamin E potentiated the effect of selenium and executed itself a similar, but less distinct effect.
通过结扎冠状动脉在大鼠中诱发心肌梗死。在一周内,它们每天接受50毫克/千克维生素E的肌肉注射或30微克/千克亚硒酸钠的皮下注射,或者这些制剂的组合。对照动物不接受注射。通过立体测量法发现,在硒的作用下梗死区域有统计学上显著的缩小,这种缩小在缺血期尤为明显;肉芽组织的成熟加速,其中成纤维细胞反应增强。梗死区域以外的心肌细胞乳酸脱氢酶活性增加,琥珀酸脱氢酶活性降低,细胞模式超微结构完整,超微结构再生迹象增强。维生素E增强了硒的作用,自身也产生了类似但不太明显的效果。