The Role of Angiotensin Converting Enzyme inhibitor in Ventricular Remodeling after Experimental Nontransmural Myocardial Infarction- Effects on Transforming Growth Factor-beta 1 Expression.
10.4070/kcj.1998.28.9.1590
- Author:
Tae Jin YOUN
;
Seok Yeon KIM
;
Hyo Soo KIM
;
Eo Jin KIM
;
So Young KIM
;
Eun Joo CHUNG
;
Jeoung Wook SEO
;
Byung Hee OH
- Publication Type:Original Article
- Keywords:
Nontransmural myocardial infarction;
Remodeling;
Transforming growth factor;
Captopril;
Losartan
- MeSH:
Angiotensins*;
Animals;
Captopril;
Coronary Occlusion;
Dilatation;
Echocardiography;
Female;
Fibrosis;
Humans;
Infarction;
Losartan;
Models, Animal;
Peptidyl-Dipeptidase A*;
Rats, Sprague-Dawley;
Receptors, Angiotensin;
Reperfusion;
RNA, Messenger;
Transforming Growth Factor beta1;
Transforming Growth Factors;
Ventricular Remodeling*
- From:Korean Circulation Journal
1998;28(9):1590-1599
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND:With the application of early reperfusion by thrombolysis after acute MI, the importance of nontransmural infarction is increasing. We evaluated 1) the changes of LV dimension, LV fibrosis and transforming growth factor-beta1 (TGF-beta1) mRNA expression in a rat model of nontransmural infarction and 2) effects of angiotensin converting enzyme inhibitor (ACEI) and angiotensin II receptor blocker (ATRB) treatment after nontransmural infarction. METHOD AND RESULTS: Female Sprague-Dawley rats were subjected to 45 minutes of coronary occlusion followed by reperfusion, and at 5 days after the operation, animals were randomized to untreated (MI-vehicle, n=19), captopril-treated (MI-captopril, n=15) and losartan-treated (MI-losartan, n=14) groups. LV dimension, measured by transthoracic echocardiography, was significantly increased at 26 days after MI, and both captopril and losartan treatment inhibited LV cavity dilatation (LV end-diastolic dimension (mm): MI-vehicle, MI-captopril, MI-losartan; 8.6 +/- 0.2, 7.8 +/- 0.2, 8.0 +/- 0.2, p<0.05 vs. MI-vehicle each). Interstitial fibrosis was reduced with both captopril and losartan treatment (p<0.05 vs. MI-vehicle). TGF-beta1 mRNA increased 2.6 fold at 10 days (p<0.05 vs. pre-MI), and normalized at 26 days after nontransmural MI. Captopril and losartan treatment blocked the induction of TGF-beta1 expression after nontransmural MI (p=S vs. pre-MI). CONCLUSION: After large nontransmural MI, ACEI and ATRB treatments attenuate LV remodeling and decrease interstitial fibrosis, at least partly by blocking the acute induction of TGF-beta1 mRNA expression.