摘要
目的缺血再灌注损伤会导致心肌细胞Na+-K+ATP酶活性降低,通过对比缺血再灌注后Na+-K+ATP酶活性改变,研究尼可地尔含血停搏液对心肌细胞Na+-K+ATP酶的保护作用。方法采用间生态离体兔心共生支持系统模型。16个心脏随机分为两组,每组8只。分别采用尼可地尔超极化含血停跳液或者高钾去极化含血停跳液灌注。超极化含血停跳液由尼可地尔(100μmol/L),Krebs-Henseleit液和兔血1:2混合配制。去极化停搏液由St.Thomas'液与兔血1:2混合配制,最终K+浓度20mmol/L。心脏停跳后以含血停跳液间断灌注,常温缺血60min。再灌注60min。采用电镜酶化学方法检测缺血前后心脏Na+-K+ATP酶的变化。结果缺血再灌注后两组中酶的活性均明显降低,高钾组较尼可地尔组减少更明显。结论尼可地尔对心肌细胞Na+-K+ATP酶缺血再灌注损伤有保护作用。
Aim The activity of myocardial Na? K?ATPase will decrease after ischemical reperfusion.The study aimed to evaluate the protective effect of the nicorandil as a blood cardioplegic agent on the myocardial Na? K?ATPase compered to the activity of Na? K?ATPase after ischemic reperfusion.Methods Using a blood perfused, parabiotic,Langendorff rabbit model,sixteen hearts from Japanese white rabbits were divided into two groups of eight subjects: nicorandil group filled with 100 μmol/L nicorandil, Krebs Henseleit and each rabbit blood mixed on 12 ratio; hyperkalemic cardioplegia group filled with St.Thomas' liquor the and rabbit blood mixed on 12 ratio with 20 mmol/L K?.Both hearts of two groups underwent 60 min normothermic ischemic perfusion and then 60 min reperfusion.The changes of Na? K?ATPase were investigated before and after cardiac ischemia by electron microscopic enzyme cytochemical technique.Results The activity of Na? K?ATPase reduced significantly after ischemia/reperfusion in both groups.The changes of the Na? K?ATPase were more obvious in the hyperkalemic cardioplegia group than those of the nicorandil group.Conclusion The nicorandil blood cardioplegia is effective in protecting the myocardial Na? K?ATPase.
出处
《中国临床康复》
CSCD
2003年第12期1752-1753,F003,共3页
Chinese Journal of Clinical Rehabilitation