目的 研究重组人脑钠肽(rhBNP)对缺血再灌注后心室肌细胞L-钙通道电流(ICa-L)的影响,并探讨其细胞学离子机制.方法 45只新西兰大耳白兔随机分为缺血再灌注动物模型组(I-R组,n=15)、rhBNP治疗组(n=15)和假手术组(n=15).采用酶解方法分离缺血部位心室肌外膜单个心室肌细胞,应用全细胞膜片钳技术记录ICa-L.结果 ①心律失常发生率:与I-R组比较,rhBNP组兔室速、室颤发生率及持续时间明显下降,而且其心律失常的评分也明显低于I-R组[(2.6±0.7) vs.(3.6±0.8),P＜0.05];②电流密度峰值:I-R组、对照组、rhBNP组ICa-L电流密度峰值(0mV)逐渐升高,分别为(-4.34±0.92) pA/pF、(-3.42±0.76)pA/pF、(-3.13±1.22)pA/pF.结论 rhBNP可降低心肌缺血再灌注期间心律失常的发生率,心肌缺血再灌注后ICa-L明显增高,rhBNP可使ICa-L下调,逆转电重构.%Objective To establish rabbit model of myocardial ischemia/reperfusion, study the influence of recombinant human brain natriuretic peptide (rhBNP) on current of ventricular myocyte L—type calcium channels ( Ica-l ) > and explore the ionic mechanism. Methods New Zealand rabbits ( n=45 ) were randomly divided into model group ( n=15 ) , treatment group ( n =15 ) and sham-operation group ( n =16 ) . Single ventricular myocytes were isolated by using enzymolysis method from ventricular epicardium in ischemia area. The current of ICa-L was recorded by using whole-cell patch clamp technique. Results ①Incidence of arrhythmia: the incidence and duration of ventricular tachycardia and ventricular fibrillation, and scores of arrhythmia all decreased significantly in treatment group compared with model group [ ( 2.6 ± 0.7 ) vs. ( 3.6 ± 0.8 ) , P<0.05]. ②The peak value of ICa-L current density ( 0 mV ) increased gradually in model group, control group and treatment groups [ ( -4.34 ± 0.92 ) pA/pF, ( -3.42 ± 0.76 ) pA/pF and ( -3.13 ± 1.22 ) pA/pF]. Conclusion During the stage of myocardial ischemia/reperfusion, rhBNP can reduce the incidence of arrhythmia. The current of ICa-L increases significantly after myocardial ischemia/reperfusion, while rhBNP can down—regulate increased ICa-L current and reverse electrical remodeling.
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