Litvitskiĭ P F, Kogan A Kh, Kudrin A N, Luk'ianova L O
Biull Eksp Biol Med. 1981 Mar;91(3):271-4.
The data obtained in experiments on 89 random bred male white rats indicate an important pathogenetic role of lipid peroxidation activation during ischemia of the myocardium and its further reperfusion. Inhibition of lipid peroxidation by sodium selenite was accompanied by increased resistance of the heart to its reversible ischemia. The evidence obtained documents a new principle of pathogenetic therapy of transitory coronary insufficiency with lipid peroxidation inhibitors, particularly sodium selenite. The data presented may be of importance for clinical practice since transitory myocardial ischemia in animals represents an experimental model of the forms of coronary heart disease of man which are accompanied by transient reduction of the coronary blood flow.
在对89只随机繁殖的雄性白鼠进行的实验中所获得的数据表明，脂质过氧化激活在心肌缺血及其后续再灌注过程中具有重要的发病机制作用。亚硒酸钠对脂质过氧化的抑制作用伴随着心脏对可逆性缺血耐受性的增强。所获得的证据证明了用脂质过氧化抑制剂（特别是亚硒酸钠）治疗短暂性冠状动脉供血不足的一种新的发病机制治疗原则。所呈现的数据可能对临床实践具有重要意义，因为动物中的短暂性心肌缺血代表了人类伴有冠状动脉血流短暂减少的冠心病形式的实验模型。
