K^+ channel opener (NICORANDIL)が心筋虚血再灌流時のcoronary flowに及ぼす影響 : ブタ開胸心筋虚血再灌流モデルによる検討

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Background: Nicorandil, a K-ATP channel opener with a nitrate-like effect, is a potent vasodilator and used clinically for the patients with angina pectoris. While its cardioprotective properties in the setting of ischemia-reperfusion are well known, the effect of nicorandil on the coronary hemodynamics during ischemia-reperfusion has not been well elucidated. The purpose of this study was to assess the effects of intravenous nicorandil during ischemia and reperfusion on the coronary flow and infarct size using an open chest pig model. Method: The left anterior descending coronary artery was occluded for 30 min. and reperfused for 150 min in open chest pigs. The pigs were randomly assigned to nicorandil reatment (NIC, n = 7), isosorbide dinitrate treatment (ISDN, n = 7) or saline treatment (control, n = 7) groups. After 15 min of coronary occlusion, nicorandil or ISDN were injected intravenously at a dose of 100 //g/kg (bolus), followed by 10 //g/kg/min continuous injection throughout the experimental protocol. In the control group, saline was injected in a same manner. Hemodynamic parameters, regional myocardial blood flow (RMBF) using colored microsphere method were measured before ischemia, during 25 min of occlusion, and 5, 30, and 120 min after reperfusion. The risk area was defined by a blue dye method and infarct size by 10% triphenyltetrazolium chloride stain. Results: There was no significant difference in the cardiac output among the groups. The pulmonary arterial pressures were slightly increased after occlusion and decreased after reperfusion in the nicorandil and ISDN groups. The systolic and diastolic blood pressures were significantly decreased after nicorandil and ISDN injection. The infarct size as a percent of the risk area was significantly smaller in the nicorandil group (2.12 + 1.17%) as compared to the control group (9.44 + 4.45% p<C0.05). The incidence of sustained ventricular tachycardia and/or fibrillation was significantly lower in the nicorandil group (28.6%) as compared to the control (100%) and ISDN (100%) groups. The RMBF in the ischemic region during 25 min of occlusion was significantly higher in the nicorandil group as compared to the control group (0.25±0.16 ml/min/g vs 0.03±0.01 ml/min/g, p<0.05). After reperfusion, the RMBF was significantly increased in all groups ( control, 2.61±0.78 ml/min/g; nicorandil, 2.03±0.85 ml/min/g; ISDN, 2.56±1.06 ml/min/g). This hyperemic RMBF decreased by time in the control and ISDN groups (1.23±0.53 ml/min/g and 1.90±0.78 ml/min/g, at 120 min after reperfusion, respectively). In the nicorandil group, however, the hyperemia sustained until 120 min after reperfusion (2.18±0.88 ml/min/g, p<0.05 vs control). Conclusion: These data suggest that nicorandil increased the collateral blood flow during ischemia even in the pig model, which is known as a model with poor collateral system and suppress the no-flow phenomenon and arrhythmia after reperfusion of the myocardium, and these beneficial effects may be attributed to the K+ channel opening mechanism of nicorandil.
愛知医科大学の論文
2004-12-10

K^+ channel opener (NICORANDIL)が心筋虚血再灌流時のcoronary flowに及ぼす影響 : ブタ開胸心筋虚血再灌流モデルによる検討

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