Szekeres L, Pataricza J, Szilvássy Z, Udvary E, Végh A
Institute of Pharmacology, Albert Szent-Györgyi Medical University, Szeged, Hungary.
Basic Res Cardiol. 1991;86 Suppl 3:215-21. doi: 10.1007/978-3-662-30769-4_21.
Evidence is accumulating that acute stress situations such as ischemia, adrenergic dominance, and ouabain intoxication enhance production of endogenous substances (PgI2, adenosine, NO) which may protect the myocardium from harmful consequences of these stress situations. PgI2 and its stable analogue 7-oxo-PgI2 exert an early direct- and induce a delayed indirect antiischemic, antiarrhythmic, and cytoprotective effect. The direct action is shortlasting; it protects from myocardial ischemia and arrhythmias, at least partly, by its vasodilating, antiaggregatory, and "membrane-stabilizing" effects. The delayed, long-lasting PgI2-induced protection from postocclusion, reperfusion- and ouabain-arrhythmias is dose- (optimal 50 micrograms/kg) and time- (optimal 48 h after treatment) dependent. Its mechanism is probably based on a 7-oxo-PgI2 induced increase in the activity of Na/K-ATP-ase, and further, on a reduced sensitivity to beta-adrenergic agonists and to changes at the cardiac membrane level, resulting in a prolongation of the action potential duration and the effective refractory period.
越来越多的证据表明，诸如缺血、肾上腺素能占优势和哇巴因中毒等急性应激情况会增强内源性物质（前列环素I2、腺苷、一氧化氮）的产生，这些物质可能保护心肌免受这些应激情况的有害后果。前列环素I2及其稳定类似物7-氧代-前列环素I2具有早期直接作用，并诱导延迟的间接抗缺血、抗心律失常和细胞保护作用。直接作用持续时间短；它至少部分地通过其血管舒张、抗聚集和“膜稳定”作用来保护心肌免受缺血和心律失常。延迟的、持久的前列环素I2诱导的对闭塞后、再灌注和哇巴因诱导的心律失常的保护作用取决于剂量（最佳剂量为50微克/千克）和时间（治疗后最佳时间为48小时）。其机制可能基于7-氧代-前列环素I2诱导的钠/钾-ATP酶活性增加，以及进一步降低对β-肾上腺素能激动剂的敏感性和心脏膜水平的变化，导致动作电位持续时间和有效不应期延长。
