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氯沙坦与赖诺普利对大鼠压力负荷性心血管重构的影响
引用本文:周俊 李东野 等. 氯沙坦与赖诺普利对大鼠压力负荷性心血管重构的影响[J]. 国外医学:心血管疾病分册, 2003, 30(1): 43-46
作者姓名:周俊 李东野 等
作者单位:江苏徐州医学院附属医院心内科 221002(周俊,李东野),江苏徐州医学院附属医院心内科 221002(陈清枝)
摘    要:
目的:探讨心血管重构的结构、功能改变以及氯沙坦和赖诺普利的干预作用。方法:膈下腹主动脉缩窄法建立大鼠心肌肥厚模型。检测各实验组平均动脉压(mean avterial pressure,MAP)、心肌肥厚程度、胸主动脉内皮功能。结果:与假手术组相比,模型组MAP、左室重量(left ventricular weight,LVW)、左室重量指数(left venticuler mess index,LVMI)、心肌细胞横径(transverse diameter of myocardium,TDM)分别提高28.6%、20.5%、26.9%、17.9%(P<0.01),胸主动脉环对乙酰胆碱(ACh)血管舒张反应明显降低(P<0.01);降压剂量氯沙坦与赖诺普利与非降压剂量氯沙坦干预后,能完全预防心肌肥厚,使胸主动脉环对ACh血管舒张反应正常化,以降压剂量氯沙坦作用最为明显;非降压剂量赖诺普利能改善心肌肥厚程度,但与假手术组有差异(P<0.01),胸主动脉环对ACh血管舒张反应无改善。六组动物胸主动脉环对硝普钠(SNP)最大舒张反应均无差别,模型组反应曲线右移。结论:氯沙坦与赖诺普利能预防心肌肥厚,改善内皮功能,与剂量有一定关系。

关 键 词:氯沙坦 赖诺普利 大鼠 压力负荷性 心血管重构 心肌肥厚

Effect of losartan and lisinopril on cardiovascular remodelling and vascular function in pressare overload rats
ZHOU Jun LI Dongye CHEN Qingzhi,et al.. Effect of losartan and lisinopril on cardiovascular remodelling and vascular function in pressare overload rats[J]. , 2003, 30(1): 43-46
Authors:ZHOU Jun LI Dongye CHEN Qingzhi  et al.
Affiliation:ZHOU Jun LI Dongye CHEN Qingzhi,et al. Dept. of Cardiology,Affiliated Hospital of Xuzhou Medical College,Jiangsu 221002
Abstract:
Objective: To investigate the stractural and functioal changes of cardiovascular remodelling in pressure overload rats and examine the preventive effects of losartan on them. Methods: Pressure overload model was produced by abdominal aortic coarctation in rats. Mean arterial pressure (MAP) and data of my-ocardial hypertrophy were measured in groups. In addition the vascular reactivity to acetylcholine (ACh) and sodium nitroprusside (SNP) was studied by using rings of thoracic. Results: As compared with Group Sham, Group model rats manifested myocardial hypertrophy. Their MAP, LVW,LVWI and TDM were 28. 6 % , 20. 5 % , 26.9 % and 17.9 % increased respectively (P < 0.01). The vascular relaxation response to ACh in Group model was decreased significantly (P<0.01). Under the interference of of lisinopril and losartan and sub-hypotensive losartan, myocardial hypertrophy may be completely prevented and the vascular relaxation response to ACh was improved. The effect of hypotensive dose losartan was most prominent. Sub-hypotensive dose lisinopril alleviated cardiovascular remodelling but did not improve vascular relaxarion response to ACh. The maximal vascular relaxation response to SNP was similar among 6 groups. The total response curve shifted to right in Group model. Conclusion: Lisinopril and losartan could prevent cardiovascular remodelling and improve vascular endothelial function,however, it is dose-dependent.
Keywords:Myocardial hypertrophy Acetylcholine Sodium nitroprusside Lisinopril Losartan  
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