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目的:探讨血管紧张素转化酶抑制剂雷米普利对兔心肌梗死后室性心律失常发生的影响及其可能机制。方法:24只家兔随机分为假手术组(SHAM)、心肌梗死组(MI)和雷米普利组(RAM)。3组均在无菌条件下开胸,其中心肌梗死组和雷米普利组分别结扎左冠状动脉前降支。雷米普利组术后第2天给予雷米普利[1mg/(kg.d)],3组共喂养12周。3组家兔分别在心肌梗死前、心肌梗死后12周记录左心室内、中、外膜层单相动作电位(MAP),并记录心肌梗死后12周诱发的恶性心律失常次数,及采用全细胞膜片钳技术记录L-型钙通道电流(Ica-L)的变化。结果:①RAM组明显降低心肌梗死后室性心动过速、心室颤动(VT/VF)的发生次数(2.6±0.8比12.4±2.9,P<0.05)。②心肌梗死后12周,MI组3层左心室肌APD90较心肌梗死前明显延长(258.2±21.1比230.1±23.2,278.0±23.8比245.8±25.4,242.6±22.7比227.0±21.7,P<0.05);RAM组3层心室肌APD90与心肌梗死前相比没有明显差异。而且,MI组跨壁复极离散度(TDR)较SHAM、RAM组明显延长(分别为36.2±10.2,18.7±6.2,24.9±8.7,P<0.05);RAM与SHAM组之间TDR比较无显著性差异。③假手术组、心肌梗死组和缬沙坦组Ica-L电流密度分别为(-6.29±0.65)pA/pF、(-9.12±0.73)pA/pF和(-7.05±0.68)pA/pF,心肌梗死组显著低于假手术组及雷米普利组(P<0.05);雷米普利组与假手术组比较无统计学差异。结论:雷米普利明显降低家兔心肌梗死后恶性室性心律失常的发生次数,其机制可能与抑制家兔心肌梗死后电重构有关。
Objective: To investigate the effect of angiotensin converting enzyme inhibitor ramipril on ventricular arrhythmia after myocardial infarction and its possible mechanism. Methods: Twenty-four rabbits were randomly divided into sham operation group (SHAM), myocardial infarction group (MI) and ramipril group (RAM). Three groups were under aseptic conditions thoracotomy, myocardial infarction group and ramipril group were ligation of left anterior descending coronary artery. Ramipril [1 mg / (kg · d)] was given on the second postoperative day in ramipril group and 12 weeks in 3 groups. Three groups of rabbits were recorded before the myocardial infarction, 12 weeks after myocardial infarction single-phase left ventricular endocardial, medial and epicardial action potential (MAP), and recorded 12 weeks after myocardial infarction induced malignant arrhythmia frequency, and the use of all Cell patch clamp technique was used to record changes in L-type calcium channel current (Ica-L). Results: (1) RAM group significantly decreased the incidence of ventricular tachycardia and ventricular fibrillation (VT / VF) after MI (2.6 ± 0.8 vs. 12.4 ± 2.9, P <0.05). ② After 12 weeks of myocardial infarction, APD90 of left ventricular muscle of 3-layer in MI group was significantly longer than that before myocardial infarction (258.2 ± 21.1 vs 230.1 ± 23.2, 278.0 ± 23.8 vs 245.8 ± 25.4, 242.6 ± 22.7 vs 227.0 ± 21.7, P <0.05) ; There was no significant difference in APD90 of RAM between the three layers of ventricular myocardium before myocardial infarction. Furthermore, the transreticular repolarization dispersion (TDR) in MI group was significantly longer than that in SHAM and RAM groups (36.2 ± 10.2, 18.7 ± 6.2, 24.9 ± 8.7, P <0.05, respectively) Sex differences. ③ The current density of Ica-L in sham group, myocardial infarction group and valsartan group were (-6.29 ± 0.65) pA / pF, (-9.12 ± 0.73) pA / pF and (-7.05 ± 0.68) pA / pF, Myocardial infarction group was significantly lower than sham operation group and ramipril group (P <0.05); ramipril group and sham operation group no statistical difference. Conclusion: Ramipril significantly reduces the incidence of malignant ventricular arrhythmias after myocardial infarction in rabbits, which may be related to the inhibition of electrical remodeling after myocardial infarction in rabbits.