地昔帕明预处理改善心肌缺血后的交感神经重构  

Desipramine Pretreatment Improves Sympathetic Remodeling after Myocardial Ischemia

作　　者：何勃[1] 江洪[1] 吴校林[1] 余锂镭[1] 赵冬冬[1] 张元元[1] 

机构地区：[1]武汉大学人民医院心内科,湖北武汉430060

出　　处：《武汉大学学报（医学版）》2009年第2期184-187,I0002,共5页Medical Journal of Wuhan University

基　　金：武汉市学科带头人计划资助项目(编号:200750730309)

摘　　要：目的:研究地昔帕明预处理对大鼠急性心肌缺血后交感神经重构的影响,并探讨室颤阈值的变化。方法:60只SD大鼠随机分为3组:心肌缺血组夹闭左冠状动脉前降支30min;地昔帕明预处理组先单次静脉给予地昔帕明0.8mg/kg,5min后夹闭左冠状动脉前降支30min;地昔帕明组夹闭左冠状动脉前降支10min后再给予地昔帕明。喂养1周后开胸测定室颤阈值,免疫组化法观察大鼠心室肌中生长相关蛋白43(GAP43)和酪氨酸羟化酶(TH)阳性神经纤维的分布和密度。结果:心肌缺血组的神经纤维分布紊乱,密度明显高于预处理组和地昔帕明组(P<0.05);其室颤阈值(7.2±1.30)V较预处理组的(11.0±2.65)V显著降低。预处理组的室颤阈值与地昔帕明组的(10.4±3.05)V相比无显著差异(P>0.05),神经纤维密度却明显降低(P<0.05)。结论:地昔帕明预处理能够改善心肌缺血后的交感神经重构,提高室颤阈值,发挥抗心律失常作用。Objective： To investigate the effect of desipramine pretreatment on sympathetic remodeling and the changes of ventricular fibrillation threshold （VFT） in rats with induced acute myocardial ischemia. Methods： Sixty SD rats were randomly assigned into three groups： myocardial ischemia group （MI, n=20）, desipramine （0.8 mg/kg） pretreatment group （DP, n=20）, and desipramine group （D, n=20）. One week after the operation, VFT was measured, and the distribution and density of growth associated protein 43 （GAP43） and tyrosine hydroxylase （TH） positive nerves in the ventricle were detected with immunohistochemical techniques. Results： The distribution of nerve fibers in MI group was chaotic, and the density was significantly higher than those in DP and D groups （P〈0.05）, while the nerve density in DP group was significantly lower than that in D group （P〈0.05）. Compared with that in DP group [（11.0 ±2.65） V], VFT of MI decreased significantly [（7.2±1.30） V] in MI group. No significant difference was found in VFT between DP and D groups （P〉0. 05）. Conclusion： Desipramine pretreatment has the antiarrhythmic effect through improving sympathetic remodeling and increasing VFT after acute myocardial ischemia.

关 键 词：地昔帕明 心肌缺血 交感神经重构 室颤阈值 

分 类 号：R541.7[医药卫生—心血管疾病]