卡维地洛联合物布他林对心肌梗死大鼠心功能影响及其作用机制-effect of carvedilol combined with budesonide on cardiac function in rats with myocardial infarction and its mechanism of action.docxVIP
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卡维地洛联合物布他林对心肌梗死大鼠心功能影响及其作用机制-effect of carvedilol combined with budesonide on cardiac function in rats with myocardial infarction and its mechanism of action
卡维地洛联合特布他林对心肌梗死大鼠心功能的影响及其作用机制 中文摘要目的 探讨卡维地洛联合特布他林对心肌梗死C心梗)后大鼠心功能的 影响,及其作用机制。 方法 结扎冠状动脉前降支制备心梗大鼠模型,术后 1 周随机分为心梗 组,卡维地洛组,联合治疗组,此外设假于术组C冠状动脉前降支穿线但不 结扎)为对照组。卡维地洛组给予卡维地洛生理水溶液 8mg/kg,一日两次灌 胃。联合治疗组给予特布他林生理水溶液 2mg/kg,卡维地洛生理水溶液 8mg/kg 一日两次灌胃。心梗组及假于术组均给予等量生理盐水,一日两次灌胃。干预 8 周后行超声心动图检查、血流动力学检测及心肌组织中谷肮甘肤、 凋亡蛋白测定。 结果①心梗组左心室舒张末期内径CLVEDd)、左室收缩末期内径CLVESd)大 于假于术组CP0.01),射血分数CEF)、短轴缩短率CFS)则低于假于术组 CP0.01)。药物治疗组较心梗组 LVEDd、 LVESd 缩小CP0.01~0.05),EF、 FS 提高CP0.01~0.05)。联合治疗组较卡维地洛组 LVEDd、LVESd 更小CP0.01),EF、FS 更高CP0.05)。 ②心梗组血流动力学指标较假于术组明显恶化(P0.01);药物干预组较 心梗组心功能指标改善(P0.01~0.05);联合治疗组较卡维地洛组心功能指 标进一步改善(P0.01~0.05)。 ③心梗组较假于术组心肌细胞凋亡蛋白CBcl-2)、还原型谷肮甘肤CGSH) 减少,氧化性谷肮甘肤CGSSG)增加CP0.01),药物治疗组较心梗组 Bcl-2、 GSH 增加,GSSG 减少CP0.01),联合治疗组较卡维地洛组 Bcl-2、GSH 增加, GSSG 减少CP0.01~0.05)。 结论 特布他林联合卡维地洛可改善心梗大鼠心功能,减轻心室重构,增加 GSH、Bcl-2 的表达。增强细胞的抗凋亡、抗氧化作用可能是其疗效提高的机制之一。 关键词 卡维地洛,特布他林,心肌梗死,心功能 The effect of combined carvedilol and terbutaline therapy on cardiac function in the myocardial infarctionrats and its mechanism AbstractObjective To investigate the effect of combined carvedilol and terbutaline therapyon cardiacfunction in the myocardial infarction(MI) rats and its mechanism.Methods The myocardial infarction rats model was prepared by ligating the anter- ior descending of coronary artery. After one week, the MI rats were randomly divided into four groups: ①the myocardial infarction group(normal saline, twice aday);② the carvedilol group(give MI rats carvedilol normal saline solution 8mg/kg, twice a day);③combined treatment group(terbutalin normal saline solution 2 mg/kg and carvedilol normal saline soluti- on 8mg/kg, twice a day);④ the sham group (the anterior descending of coronary artery threading but not ligation). After 8 weeks of remedy, echo- cardiographic and hemodynamic was conducted, thenGSH、GSSG and apoptosis protein(Bcl-2) was deterinined in myocardial cells.ResultsCompared with the sham group, left ventricular end-diastolic diameter (LVED d)、left ventri- cular end-systolic diameter (LVESd) were increased(P0.
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