贵州医科大学学报

2008, No.131(02) 115-117

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比索洛尔和卡维地洛对大鼠缺血心肌血管新生的影响
The Effects of Bisoprolol and Carvedilol on Angiogenesis in Ischemic Myocardium of Rats

刘兴德;张蕊;
LIU Xingde,ZHANG Rui(Department of Cardiac Internal Medicine,The Affiliated Hospital of Guiyang Medical College,Guiyang 550004,Guizhou,China)

摘要(Abstract):

目的:观察比索洛尔和卡维地洛是否具有促大鼠缺血心肌血管新生的作用。方法:运用大鼠心肌缺血模型,分别给予比索洛尔和卡维地洛灌胃并记录心率。用免疫组织化学方法检测大鼠缺血心肌中毛细血管密度(CD)和内皮细胞(EC)的表达。结果:与模型组比较,比索洛尔组大鼠缺血心肌CD和EC数均明显增加(P<0.01),其心率明显降低(P<0.01);与模型组比较,卡维地洛组大鼠缺血心肌CD、EC数以及心率均无显著性差异。结论:比索洛尔能促进大鼠缺血心肌的血管新生其减慢心率可能是比索洛尔促进大鼠缺血心肌血管新生的机制之一。
Objective:To observe whether bisoprolol and carvedilol could promote angiogenesis in ischemic myocardia of rat.Methods:Fifty-four myocardium infarction model rats established for 1 week were divided randomly into bisoprolol group(treated with bisoprolol),carvedilol group(treated with carvedilol) and control group(treated with physiologic saline),and were further divided into subgroups of A1,A2,A3,B1,B2,B3,C1,C2,and C3 which were executed in 1 week,2 weeks,and 3 weeks respectively.Their heart rates were recorded and the capillary density(CD) and endothelial cell(EC) in their myocardia were detected by using immunohistochemical methods.Results:Compared with those of control group,the numbers of CD and EC in rats of bisoprolol groups were significantly bigger,and their heart rates were significantly lower;The numbers of CD and EC,and heart rates in rats of carvedilol groups did not differ significantly from those in rats of control groups.Conclusions:Bisoprolol may promote angiogenesis in ischemic myocardium of rats,in which process the decreasing of heart rate may be one of the mechanisms.

关键词(KeyWords): 心肌缺血;毛细血管;冠状动脉疾病;比索洛尔;卡维地洛
myocardial ischemia;capillaries;coronary disease;bisoprolol carvedilol

Abstract:

Keywords:

基金项目(Foundation): 教育部科学技术研究重点项目(204128)

作者(Author): 刘兴德;张蕊;
LIU Xingde,ZHANG Rui(Department of Cardiac Internal Medicine,The Affiliated Hospital of Guiyang Medical College,Guiyang 550004,Guizhou,China)

Email:

DOI: 10.19367/j.cnki.1000-2707.2008.02.002

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