Warltier D C, Auchampach J A, Gross G J
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226.
J Card Surg. 1993 Mar;8(2 Suppl):279-83. doi: 10.1111/j.1540-8191.1993.tb01323.x.
Pharmacological modulation of ATP sensitive potassium channels (K+ATP channels) in vivo may influence ischemia and reperfusion injury of myocardium. The purpose of this investigation was to ascertain the actions of multiple K+ATP channel openers and interactions with a K+ATP channel antagonist in a model of stunned myocardium in anesthetized and conscious dogs. The results indicate that the K+ATP channel openers, aprikalim and nicorandil, enhance recovery of regional contractile function of stunned myocardium. This action was blocked by the selective K+ATP antagonist, glyburide. The beneficial effects of K+ATP channel openers were not related to changes in systemic hemodynamics or coronary collateral perfusion, but instead may be a manifestation of direct cardioprotective actions of these compounds.
体内对ATP敏感性钾通道（K⁺ATP通道）进行药理调节可能会影响心肌的缺血和再灌注损伤。本研究的目的是在麻醉和清醒犬的心肌顿抑模型中确定多种K⁺ATP通道开放剂的作用以及与一种K⁺ATP通道拮抗剂的相互作用。结果表明，K⁺ATP通道开放剂阿普卡林和尼可地尔可增强心肌顿抑区域收缩功能的恢复。这种作用被选择性K⁺ATP拮抗剂格列本脲阻断。K⁺ATP通道开放剂的有益作用与全身血流动力学或冠状动脉侧支灌注的变化无关，而可能是这些化合物直接心脏保护作用的一种表现。
