THE ROLE OF ATP-SENSITIVE POTASSIUM CHANNELS IN THE MECHANISMS OF METABOLIC CORONARY VASODILATION

（1）格列本克拉胺（ATP敏感性钚通道的抑制剂）对代谢电晕挥发性实验的影响在无意识和有意识的狗中表现。从100 - 160 bpm增加心脏速率，而无需改变其他血动力学参数。格列本克拉胺（1.5和5.0 mug/kg·min）被pacing tachycardia明显抑制了冠状挥发性，但当它没有影响冠状挥发性被乙酰胆碱素和硝酸甘油素诱导。格列本克拉胺完全被用吡酸地il废除了冠状挥发性诱导。这些结果建议代谢冠状挥发性最少在ATP敏感性钙通道的部分中被介导。2）对吡啶（ATP敏感性钙通道开放器）的影响（ATP敏感性钙通道）在代谢冠状挥发性实验中表现得很好。肾上腺素的内源性灌注（一种选择性的β 1-肾上腺素抑制剂）与心肌梗死的原发性异位状态中的增加有关的冠状血流。吡啶1 mug/min，因为对碱性血红素参数没有影响，但适度增加了10%或更少的冠状血液流动，增强了脱氧胺的冠状挥发诱导，而脱氧胺诱导的改变在肌钙中性状态和肌钙氧消耗可以比较之前和之后。吡啶并不影响coronary vasodilation诱导的乙酰胆碱素， nitroglycerin和beta2-肾上腺素刺激。二氮胺诱导的冠状挥发性药物完全被一种选择性β 1肾上腺素拮抗剂双氮洛尔抑制。这些结果提出了一个由beta1-肾上腺素刺激诱导的ATP敏感性钾通道启用的吡啶酰增强的代谢冠状挥发性。

1) Effects of glibenclamide (an inhibitor of ATP-sensitive potassium channels) on metabolic coronary vasodilationExperiments were performed in anesthetized and conscious dogs. Increasing heart rate from 100 to 160 bpm increased coronary blood flow without altering other hemodynamic parameters. Glibenclamide (1.5 and 5.0 mug/kg・min) significantly inhibited coronary vasodilation induced by pacing tachycardia, while it did not affect coronary vasodilation induced by acetylcholine and nitroglycerin. Glibenclamide completely abolished coronary vasodilation induced by pinacidil. These results suggest that metabolic coronary vasodilation is mediated at least in part by ATP-sensitive potassium channels.2) Effects of Pinacidil (ATP-sensitive potassium channel opener) on metabolic coronary vasodilationExperiments were performed in anesthetized dogs. Intracoronary infusion of denopamine (a selective beta1-adrenoceptor agonist) increased coronary blood flow associated with an increase in myocardial inotropic state. Pinacidil 1 mug/min, that had no effects on basal hemodynamic parameters but modestly increased coronary blood flow by 10% or less, augmented coronary vasodilation induced by denopamine, while denopamine-induced changes in myocardial inotropic state and myocardial oxygen consumption were comparable before and after pinacidil.Pinacidil did not affect coronary vasodilation induced by acetylcholine, nitroglycerin, and beta2-adrenoceptor stimulation. Denopamine-induced coronary vasodilation was completely inhibited by a selective beta1 adrenoceptor antagonist bisoprolol. These results suggest that ATP-sensitive potassium channel opener pinacidil augments metabolic coronary vasodilation induced by beta1-adrenoceptor stimulation.