Abstract
The aim of the present study was to investigate the effects of spironolactone and losartan on the early healing stage of acute myocardial infarction (AMI) in rats. An AMI rat model was established and the rats were randomly divided into four groups: AMI (n=12), AMI + spironolactone (AMI + S; n=12), AMI + losartan (AMI + L; n=12) and AMI + spironolactone combined with losartan (AMI + S + L; n=12). Sham-operated rats served as a control group (n=12). The expression levels of matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMPs) in the non-infarcted myocardium surrounding the AMI area were determined using immunohistochemistry. In addition, the capillary density in the non-infarcted myocardium surrounding the AMI area was detected. The capillary densities around the infarcted area in the AMI and treatment groups at day 7 and 14 following AMI surgery were significantly higher compared with the sham-operated rats. Compared with the AMI group, the capillary densities around the infarcted area and the ratio of MMPs/TIMP-1 were increased in the treatment groups following AMI surgery; however, the increased ratio of MMPs/TIMP-1 was reduced at day 14 following AMI surgery. Therefore, these results indicated that spironolactone and losartan may promote the formation of collateral circulation in the non-infarcted tissue surrounding the infarcted area by regulating the production of MMPs.
Highlights
Numerous studies have demonstrated that aldosterone is an important etiology of myocardial fibrosis and cardiac remodeling following myocardial infarction [1,2,3,4]
At day 7 and 14 following acute myocardial infarction (AMI) surgery, the rats treated with spironolactone and/or losartan presented higher capillary density in the non‐infarcted tissue around the infarcted area when compared with the AMI or sham‐operated groups (Table I)
The present study investigated the effects of higher doses of aldosterone receptor antagonist and angiotensin 1 (AT1) receptor antagonist in the inhibition of vascularization in the surrounding area of the infarcted area
Summary
Numerous studies have demonstrated that aldosterone is an important etiology of myocardial fibrosis and cardiac remodeling following myocardial infarction [1,2,3,4]. These drugs may be used as an alternative for angiotensin‐converting enzyme inhibitors in the treatment of heart failure
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