Effects of complete heart block on myocardial function, morphology, and energy metabolism in the rat
Effects of complete heart block on myocardial function, morphology, and energy metabolism in the rat
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DOI：
10.1093/europace/eum065
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发表时间：
2007-06-01
期刊：
影响因子：
6.1
通讯作者：
Omerovic, E.
中科院分区：
文献类型：
--
作者：
Gizurarson, S.;Lorentzon, M.;Omerovic, E.
目的严重的持续性心动过缓可引起急性和慢性充血性心力衰竭（CHF）。本研究的目的是研究完全心脏传导阻滞（CHB）对心功能、形态和肌酸（Cr）代谢的急性和慢性影响。方法与结果采用房室结区电灼法制备雄性sd大鼠（250 g, n = 11），并与对照组（n = 15）进行比较。在CHB诱导后1周、3周和12周用经胸超声心动图对大鼠进行观察。有创血流动力学评估左、右心室压力在12周。牺牲后，将心脏冷冻夹紧，分析心肌Cr和高能磷代谢产物。手术有效率为54%。围手术期死亡率为20%。CHB大鼠心率（HR）降低50% (P < 0.01)，脑卒中容积（SV）增加2.5倍（P < 0.01）。心脏指数保持不变。CHB大鼠生长正常，没有明显的痛苦。左、右心室充盈压力正常。CHB大鼠出现明显的心功能异常，双室扩张和偏心左室肥厚（P < 0.01）。心肌Cr和高能磷代谢产物含量无明显变化。结论慢性乙型肝炎大鼠的血流动力学和生化特征不符合慢性乙型肝炎大鼠血流动力学和生化特征。该模型可用于研究慢性乙型肝炎和心动过缓对心肌结构、功能、电生理和代谢的影响，以及细胞治疗修复房室传导的研究。
Aims Severe sustained bradycardia may cause acute and possibly chronic congestive heart failure (CHF). The aim of this study was to investigate acute and chronic effects of complete heart block (CHB) on cardiac function, morphology, and creatine (Cr) metabolism.Methods and results CHB was induced in mate Sprague-Dawley rats (similar to 250 g, n = 11) by means of electrocautery applied to the region of AV node and were compared with controls (n = 15). The rats were investigated at 1, 3, and 12 weeks after CHB induction with transthoracic echocardiography. Invasive haemodynamic assessment of left and right ventricular pressures was performed at 12 weeks. After the sacrifice, the hearts were freeze-clamped for analysis of myocardial Cr, and high energy phosphometabolites. The efficacy of operative procedure was 54%. The peri-operative mortality rate was 20%. Heart rate (HR) decreased by similar to 50% (P < 0.01) while stroke volume (SV) increased 2.5 times (P < 0.01) in the CHB rats. Cardiac index remained unchanged. The rats with CHB grew normally and were in no apparent distress. Filling pressures in left and right ventricles were normal. The CHB rats developed marked cardiornegaly with biventricular dilatation and eccentric left ventricular hypertrophy (P < 0.01). There was no change in the myocardial content of Cr and high energy phosphometabolites. Conclusion Rats with CHB are compensating for reduction in FIR with increased SV without haemodynamic and biochemical characteristics of CHF. This model may be useful to study the effects of CHB and bradycardia on myocardial structure, function, etectrophysiotogy, and metabolism as well as for studies of cell therapy for reparation of AV conductance.