摘要
目的:观察钾离子通道开放剂加入St.Thomas Ⅱ液内,能否改善缺血后未成熟心肌的保护作用。 方法:未成熟新西兰大耳白兔(2~3周)24只随机分为对照组、处理组和预处理组(各组n=8),取离体心脏乳头肌标本。对照组充氧台氏液灌注平衡60分,StThomas Ⅱ号液灌注停跳30分,充氧台氏液复灌60分。处理组将钾离子通道开放剂Nicorandil加入StThomas Ⅱ号液灌注停跳30分。预处理组使用特异性钾离子通道阻滞剂Glibenclamide在平衡期后15分预处理乳头肌标本。利用传统玻璃微电极技术记录心肌细胞动作电位变化。 结果:①处理组乳头肌停跳后静息电位低于对照组和预处理组,有显著性差异(P<0.05=。②处理组停跳时间短于其他2组,有显著性差异(P<0.05=。③复灌早期处理组50%动作电位时程(APD50、)、90%动作电位时程(APD90)短于停跳前,有显著性差异(P<0.01=,而对照组和预处理组APD50、APD90都明显延长,有显著性差异(P<0.05=,但2组间无显著性差异。④再灌注后处理组动作电位振幅(APA)。
Objective:To observe St Thomas Ⅱ Solution enriched potassium channel opener nicorandil might enhance immature myocardial protection after myocardial hypoxia Methods:Twenty four immature New Zealand White rabbit were randomly divided into three groups(n=8) In control group,cardioplegia was St Thomas Ⅱ In treatment group,cardioplegia was addition with potassium channel opener nicorandil in St Thomas Ⅱ In pretreatment group,pretreatment was the specific potassium channel blocker glibenclamide 15 minute before arrest used nicorandil cardioplegia We tested myocardial electrophysical before and after cardioplegic arrest in immature rabbit papillary muscle preparations Results:①Resting potential was significantly decreased during arrest in treatment group(p<0.05) ②Time to arrest was shortened significantly in treatment group(p<0.05) ③In early reperfusion,APD50and APD90were significantly reduced in treatment(p<0.01),but APD50and APD90were significantly prolonged in control group and in pretreatment group(p<0.05),there were no discrepancy between the two groups ④In treatment group,the rate of recovery of APA?OS or Vmax was higher than other two groups during reperfusion(p<0.05) Conclusion:Nicorandil cardioplegic solution induces hyperpolarize arrest and enhances the immature myocardial protection after hypoxic period
出处
《中国循环杂志》
CSCD
北大核心
2001年第6期472-474,共3页
Chinese Circulation Journal