Meerson F Z, Saltykova V A, Didenko V V, Savov V M, Kagan V E
Kardiologiia. 1984 May;24(5):61-8.
In the initial phase of its action on the contracting myocardium the inductor of lipid peroxidation (LPO) H2O2 displays marked positive ino- and chronotropic as well as relaxant effects which are, therefore, close to catecholamine effects. Since catecholamines activate LPO it suggests that such activation may be involved in the mechanism of their physiologic action. The prolongation of H2O2 action inevitably leads to the development of bradycardia and bradyarrhythmic arrhythmia which may ultimately end in cardiac arrest. The atrial resistance to H2O2 in animals exposed to stress is considerably diminished: in response to this inductor of LPO such animals develop more pronounced bradyarrythmic arrhythmia and cardiac arrest without the stage of the initially positive inotropic effect. The preincubation of the contracting atrium by HP-6, a LPO inhibitor of the hydroxypyridine class, checks the development of bradyarrhythmic arrhythmia and in many cases prevents cardiac arrest. Taken as a whole these data suggest that LPO activation may play an important role in the pathogenesis of cardiac rhythm disorders which may serve as substantiation for the use of antioxidants in the treatment and prevention of arrhythmias.
在脂质过氧化（LPO）诱导剂H₂O₂作用于收缩心肌的初始阶段，它呈现出显著的正性变力、变时以及舒张作用，因此这些作用与儿茶酚胺的作用相近。由于儿茶酚胺会激活LPO，这表明这种激活可能参与了它们的生理作用机制。H₂O₂作用的延长不可避免地会导致心动过缓和缓慢性心律失常的发生，最终可能导致心脏骤停。在遭受应激的动物中，心房对H₂O₂的耐受性显著降低：作为LPO诱导剂的反应，此类动物会出现更明显的缓慢性心律失常和心脏骤停，而没有最初正性变力作用的阶段。用羟基吡啶类LPO抑制剂HP - 6对收缩的心房进行预孵育，可抑制缓慢性心律失常的发展，并且在许多情况下可预防心脏骤停。总体而言，这些数据表明LPO激活可能在心律失常的发病机制中起重要作用，这可以作为使用抗氧化剂治疗和预防心律失常的依据。
