氯沙坦与赖诺普利对大鼠压力负荷性心血管重构的影响 |
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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. |
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作者姓名: | 周俊 李东野 |
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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) |
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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。
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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 |
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Authors: | ZHOU Jun LI Dongye CHEN Qingzhi |
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Institution: | ZHOU Jun LI Dongye CHEN Qingzhi,et al. Dept. of Cardiology,Affiliated Hospital of Xuzhou Medical College,Jiangsu 221002 |
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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. |
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Keywords: | Myocardial hypertrophy Acetylcholine Sodium nitroprusside Lisinopril Losartan |
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