CHRONIC EFFECTS OF EARLY ANGIOTENSIN-CONVERTING ENZYME INHIBITOR (QUINAPRIL) OR ANGIOTENSIN II RECEPTOR BLOCKADE (LOSARTAN) ON HEMODYNAMICS AND REMODELING IN RATS AFTER EXPERIMENTAL MYOCARDIAL INFARCTION

The long-term effects of an angiotensin-converting enzyme (ACE) inhibitor on hemodynamics and remodeling

What is the optimal initiation timing of angiotensin converting enzyme inhibitor treatment for maximum benefits in acute myocardial infarction patients？

Randomized clinical trials led to the clinical recommendation that angiotensin-converting enzyme inhibitors （ACEI） should be used as standard therapy in most patients experiencing an acute myocardial infarction （AMI）. However, the optimal initiation timing of treatment, as well as the exact mechanisms, have not been completely resolved, especially with the development of reperfusion strategy after AMI. Earlier initiation of ACEI might be associated with more prompt recovery of left ventricular ejection fraction due to more rapid attenuation of negative remodeling.

Role of Bradykinin on Left Ventricular Remodeling and Cardiac Function after Myocardial Infarction in Rats

Objectives To investigate the influences of bradykinin （BK） on hemodynamics, left ventricular hypertrophy and interstitial collagen metabolism after myocardial infarction （MI） in rats and the contribution of BK in angiotensin-converting enzyme （ACE） inhibition therapy. Methods By means of hemodynamic measurements, morphometric study of myocyte hypertrophy and SDS-PAGE technique, the effects of enalapril （500 μg.kg^-1.day^-1 ）, enalapril （500 μg.kg^-1.day^-1） with BK B2 receptor antagonist Hoe-140 （500 μg . kg^-1.day^-1）, angiotensin Ⅱ （AgⅡ） type 1 （AT1） receptor antagonist losartan （3 mg.kg^-1.day^-1 ） on mean arterial pressure （MAP）, left ventricular end-diastolic pressure （LVEDP）, as well as maximum positive left ventricular pressure change （ ＋ dp/dtmax）, V（m） n, collagen content and the ratio of type Ⅰ to type Ⅲ collagen （ Ⅰ / Ⅲ ） of noninfarcted area were observed in rats after MI. Treatments were started on the 3rd day after MI and continued for another 28 days. Results Enalapril reduced LV- EDP, V （m） n and collagen content as well as collagen Ⅰ /Ⅲ compared with the untreated MI group （ P 〈 0. 05 ）, and all of these effects of enalapril were partly blunted by concomitant treatment with hoe-140 （ P 〈 0. 05 ）. Losartan was less effective than enalapril （P 〈 0. 05 ）. However, three treatment groups had no significant differences in ＋ dp/dtmax and had similar reductions in MAP compared with untreated MI group. Conclusions BK can improve cardiac function and prevent left ventricular hypertrophy with myocardial fibrosis independent of blood pressure. The mechanisms of ACEI are both blockade of Ang Ⅱ formation and inhibition of BK degradation.

缺失型血管紧张素转换酶基因与心肌梗塞的关系

目的：探讨缺失型（ＤＤ）血管紧张素转换酶（ＡＣＥ）基因与冠心病的相关性。方法：收集５５例心肌梗塞患者及４７例附照组，用 ＰＣＲ技术检测 ＡＣＥ基因缺失／插入多态性。结果：心肌梗塞组 ＡＣＥ ＤＤ、Ｄ基因频率分别为 ０．８０、０．８７较对照组 ０．８３，０．８３无显著统计学差异（Ｐ＞０．０５）。结论：缺失型ＡＣＥ基因可能与冠心病发病无关联。

血管紧张素转化酶基因多态性与心肌梗死的相关研究

目的：了解血管紧张素转化酶（ａｎｇｉｏｔｅｎｓｉｎ ｃｏｎｖｅｒｔｉｎｇ ｅｎｚｙｍｅ， ＡＣＥ） 基因的插入／缺失（ｉｎｓｅｒｔｉｏｎ／ｄｅｌｅｔｉｏｎ，Ｉ／Ｄ）多态性在中国人群中与心肌梗死（ 简称心梗）是否相关。方法：选择了１５０ 例住院心梗病人为实验组，１５０ 例住院的非心血管病患者作对照， 抽取外周静脉血提取ＤＮＡ，同时所有研究对象记录其病史、体检等临床资料及吸烟、饮酒等流行病学资料，应用ＰＣＲ 进行ＡＣＥ 的基因型分析。结果：Ｉ等位基因和Ｄ 等位基因频率在心梗组分别为０ ．５８ 和０ ．４２ ，在对照组为０ ．６５ 和０．３５。基因型频率的分布符合ＨａｒｄｙＷｅｉｎｂｅｒｇ 平衡。在全体研究的样本中，未发现ＩＤ或ＤＤ 基因型与心梗相关；但在年龄小于或等于６０ 岁的个体中，ＤＤ 基因型与心梗显著相关（ＯＲ＝ ２ ．３３ ，９５％ ＣＩ：１．２０４ ．５７）。并且这一相关性在年龄６０ 岁及以下且肥胖的个体中进一步增强。结论：在研究的样本中，未发现ＡＣＥ基因型与心梗相关；但在年龄６０ 岁及以下的个体中，ＤＤ基因型与心梗显著相关，且这种相关在合并肥胖的个体中进一步加强。

心肌梗塞患者血管紧张素转换酶基因缺失多态性分析

血管紧张素转换酶（ＡＣＥ）基因的多态性被认为与血浆ＡＣＥ浓度有关，同时也是欧洲人群心肌梗塞的独立的危险因子，尤其是那些一般被认为是心肌梗塞低危者。作者应用ＡＣＥ基因内含于１６多态区两侧的序列作为引物，用多聚酶链反应方法来检测ＡＣＥ基因多态性，对中国人中４０例心肌梗塞患者和４０例非冠心病患者进行了比较，结果表明心肌梗塞患者中ＤＤ基因型发生率（５０％）明显高于对照组（２０％）．在中国人中ＡＣＥ／ＤＤ基因型可能是心肌梗塞的重要危险因子。