期刊文献+

氯沙坦、培多普利对大鼠急性心肌梗死后心室重构及血流动力学的干预作用

Effects of losartan and perindopril on ventricular remodeling and left ventricular function after AMI in rats
下载PDF
导出
摘要 目的观察氯沙坦、培多普利对大鼠急性心肌梗死(AMI)后心脏大体形态和血流动力学的影响。方法 结扎左冠状动脉法制作AMI模型,随机分为对照组(C);氯沙坦组(L);培多普利组(P);氯沙坦加培多普利组(LP);假手术组(S)。6周后观察心脏长径、周径、左心室重量、心率、血压、左心室收缩压(LVSP)、左心室舒张末期压(LVEDP)和±ap/at等指标。结果①3个用药组的动脉收缩压(SBP)、舒张压(DAP)和动脉平均压(MBP)及LVSP显著低于S和C组(P<0.01及P<0.05);②与S组比较,C组(P<0.001)和3个用药组(P<0.05)的LVEDP显著增高,而±dp/dt(P<0.01)显著降低,且3个用药组的LVEDP明显低于C组,而±dp/dt显著高于C组(P<0.01);③C组的心脏长径、周径、左室重量及左室重量指数显著高于S组和3个用药组(均P<0.05)。结论氯沙坦、培多普利可以减轻左室重构,改善心功能障碍。 OBJECTIVE: To investigate the effects of losartan and perindopril on ventricular remodeling and left ventricular function after AMI in rats. METHODS: Animal models of AMI were made in rats and randomly divided into 5 groups: sham-operated group (S), control (C), losartan treatment (L), perindopril treatment (P), and combined treatment (LP). After 6 weeks, the heart length, periphery, left ventricular weight, heart rate, blood pressure, left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP) and ± dp/dt were measured. RESULTS: The SBP, SDP, MAP and LVSP were significantly decreased in all the treated groups (P < 0.01 or P < 0.05). Compared with S group, LVEDP was significantly increased in C (P < 0.001) and the treated groups (P < 0.05), ± dp/dt was significantly decreased (P < 0.01). LVEDP in the treated groups was lower than that in C group (P < 0.01). ± dp/dt in the treated groups was higher than that in C group (P < 0.01). The heart length and periphery and left ventricle weight were significantly increased in C groups (P < 0.05). CONCLUSION: Losartan and Perindopril could improve the left ventricular remodeling and heart functions in AMI rats.
出处 《中国药学杂志》 EI CAS CSCD 北大核心 2004年第9期670-672,共3页 Chinese Pharmaceutical Journal
关键词 氯沙坦 培多普利 急性心肌梗死 左室重构 血流动力学 Cardiology Functions Mathematical models Random processes
  • 相关文献

参考文献9

  • 1[1]Goldstein S, Ali AS, Sabbah H, et al. Ventricular remodeling. Mechanisms and prevention[ J]. Cardiol Clin, 1998,16:623.
  • 2[2]Solomon SD, Pfeffer MA. Myocardial infarction, ventricular remodeling,and angiotensin-converting enzyme inhibition: Where we stand today[J]. Am Heart J, 1998,136:931.
  • 3[3]Olivetti G, Capasso JM, Megga LG, et al. Cellular basic of chronic ventricular remodeling after myocardial infarction in rats [J] . Circ Res, 1991,68:856.
  • 4[4]Liu YH, Yang XP, Sharov VG, et al. Effects of angiotensin-converting enzyme inhibitors and angiotensin Ⅱ type 1 receptor antagonists in rats with heart failure: Role of kinins and angiotensin Ⅱ type 2 receptors [J]. J Clin Invest, 1997,99:1926.
  • 5[5]Wollert KC, Studer R, Bulow BV, et al. Survivl after myocardial infarction in the rat: role of tissue angiotensin-converting enzyme inhibition[J]. Circulation, 1994,90:2457.
  • 6[6]Nishikimi T, Yamagishi H, Takeuchi K, et al. An angiotensin Ⅱ receptor antagonist attenuates left ventricular dilatation after myocardial infarction in hypertensive rats[ J]. Cardiovas Res, 1995,29: 856.
  • 7[7]Kohya T, Yokoshiki H, Tohse N, et al. Regression of left ventricular hypertrophy prevents ischemia-induced lethal arrithymias: Beneficial effect of angiotensin Ⅱ blockade [J]. Circ Res, 1995,76: 892.
  • 8[8]Ju H, Zhao S, Dasvinder S, et al. Effect of AT1 receptor blockade on cardiac collagen remodeling after myocardial infarction [J]. Cardiovasc, 1997,35:223.
  • 9[9]Mulder P, Devaux B, Richard V, et al. Early versus delayed angiotensinconverting enzyme inhibition in experinental chronic heart failure:effect on survival, hemodynamics, and cardiovascular remodeling[J]. Circulation, 1997,95:1314.

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部