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

Hai-zhu ZHANG; Li-quan LEI; Chang-cong CUI; Jian LIU

摘要：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-con-verting enzyme (ACE) inhibition therapy. Methods By means of hemodynamic measurements, morphometric study of myocyte hypertrophy and SDS-PAGE technique ,the effects of enalapril pressure (500μg·kg-1·day-1) ,enalapril(500μg·kg-1·day-1) with BK B2 receptor antagonist Hoe-140 (500μg·kg-1·day-1),angiotensin Ⅱ (AgII) type 1 (AT1) receptor antagonist losartan(3mg·kg-1·day-1)on mean arterial pressure (MAP) ,left ventricular end-dias-tolic pressure (LVEDP), as well as maximum positive left ventricular pressure change (+ dp/dtmax), Ⅴ(m) n, col-lagen 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.