Development of the pharmacological post conditioning via positive inotropics and elucidation of the intracellular mechanism

本研究旨在确定两种正性肌力药物（米力农和左西孟旦）是否发挥心脏保护作用，并阐明其细胞内机制。米力农和左西孟旦均能显著缩小缺血刺激后的心肌梗死面积。磷脂酰肌醇-3-激酶和一氧化氮是这些药物的心脏保护作用的共同介质。蛋白激酶C、环氧合酶2和线粒体ATP敏感性钾通道在左西孟旦诱导的心脏保护中起关键作用。

The present study was carried out to determined whether two inotropics(milrinone and levosimendan), which have positive inotropic effects despite different mechanisms, exert cardioprotective effects and to elucidate their intracellular mechanisms. Both milrinone and levosimendan significantly decreased the myocardial infarct size after ischemic stimulus significantly. Phosphatidylinositol-3-kinase and nitric oxide were common mediators for the cardioprotection of these drugs. Protein kinase C, cyclooxygenase 2, and mitochondrial ATP sensitive potassium channels played crucial roles in levosimendan-induced cardioprotection.