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AT1受体拮抗剂和ACEI对MI后心室重构作用的比较
引用本文:车京津,张承宗. AT1受体拮抗剂和ACEI对MI后心室重构作用的比较[J]. 中国心血管杂志, 2002, 7(5): 372-375
作者姓名:车京津  张承宗
作者单位:天津医科大学第二医院,天津,300211
摘    要:心肌梗死 ( myocardial infarction,MI)后心室重构对 MI患者的预后具有深远的影响。 MI后循环和心脏局部组织中的肾素 -血管紧张素系统 ( renin-angiotensin system ,RAS)被激活 ,在刺激全身和心脏局部产生代偿反应的同时 ,也带来危害——心肌肥厚和间质纤维化。应用血管紧张素转换酶抑制剂 ( angiotensin converting enzyme inhibitor,ACEI)阻断这一系统 ,已显示出具有防止心脏重构、延长患者生存时间的作用。其作用主要归因于抑制循环及局部血管紧张素 ( angiotensin ,Ang )的生成 ,以及减少缓激肽 ( bradykinin,BK)的降解。与 ACEI相比 ,选择性 1型血管紧张素 受体 (简称 AT1受体 )拮抗剂在理论上能够更加长期、有效地阻断血管紧张素 通过其 1型受体发挥的作用 ,且其作用并不仅限于此。

关 键 词:心肌梗死  心室重构  血管紧张素转换酶抑制剂  选择性1型血管紧张素Ⅱ受体拮抗剂
修稿时间:2000-05-05

Comparative effects of angiotensin Ⅱ type 1 receptor antagonists and ACEI on ventricular remodeling after myocardial infarction
Che Jingjin,Zhang Chengzong. Comparative effects of angiotensin Ⅱ type 1 receptor antagonists and ACEI on ventricular remodeling after myocardial infarction[J]. Chinese Journal of Cardiovascular Medicine, 2002, 7(5): 372-375
Authors:Che Jingjin  Zhang Chengzong
Abstract:Postinfarcted ventricular remodeling has a profound influence on the prognosis of patients with MI. Circulatory and cardiac tissue renin-angiotensin systems (RAS) are activated after MI, which not only stimulate the compensatory reaction, but also bring about some harmful results, mainly including myocardial hypertrophy and interstitial fibrosis. Blocking this system with ACEI has shown to prevent cardiac remodeling and to prolong survival of patients with MI. This beneficial effect of ACEI are mainly attributed to inhibiting the production of Ang Ⅱ in circulation and cardiac tissue, as well as decreasing the breakdown of bradykinin. Contrasting with ACEI, selective Ang Ⅱ type 1 receptor (AT1 receptor) antagonists are theoretically capable of longer and more effectively blocking the effects of Ang Ⅱ exerted via AT1 receptor, furthermore their effects are not limited to the above.
Keywords:Myocardial infarction  Ventricular remodeling  Angiotensin converting enzyme inhibitor  Selective AT1 receptor antagonist
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