EFFECT OF PROLONGED BETA-ADRENERGIC-BLOCKADE INDUCED BY ATENOLOL ON LEFT-VENTRICULAR REMODELING AFTER ACUTE MYOCARDIAL-INFARCTION IN THE RAT

Citation
K. Shimada et al., EFFECT OF PROLONGED BETA-ADRENERGIC-BLOCKADE INDUCED BY ATENOLOL ON LEFT-VENTRICULAR REMODELING AFTER ACUTE MYOCARDIAL-INFARCTION IN THE RAT, Japanese Heart Journal, 36(1), 1995, pp. 81-89
Citations number
NO
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
00214868
Volume
36
Issue
1
Year of publication
1995
Pages
81 - 89
Database
ISI
SICI code
0021-4868(1995)36:1<81:EOPBIB>2.0.ZU;2-6
Abstract
Beta-adrenergic receptor blockade reduces the mortality rate after acu te myocardial infarction (AMI) in humans. However, the effects of beta blockade on left ventricular remodeling remain unknown. Therefore, in the present study we investigated the effect of prolonged beta-adrene rgic receptor blockade with atenolol on left ventricular remodeling fo llowing AMI in rats. Myocardial infarction (MI) was produced in Wistar -Kyoto rats by ligating the coronary artery. Four groups of rats were studied: sham-operated (n = 10); atenolol (1 g/l in drinking water) tr eated sham-operated (n = 8); untreated MI (n = 11); atenolol treated M I (n = 10). Hemodynamic measurements were made about 3 weeks after the operation. Infarct size was similar in treated and untreated MI rats (31.2 +/- 2.5% cf. 33.5 +/- 2.0%). MI rats were characterized by incre ases in left ventricular end-diastolic pressure (LVEDP), right atrial pressure (RAP), right ventricular systolic pressure (RVSP), and left v entricular end-diastolic volume index (LVEDVI), as compared with sham- operated rats. In sham-operated rats, prolonged beta-adrenergic recept or blockade produced only a reduced HR. Atenolol-treated MI rats had a significantly higher LVEDP, RAP and LVEDVI than did rats with untreat ed MI. Prolonged beta-adrenergic receptor blockade with atenolol appea red to promote left ventricular remodeling after AMI. Thus, the treatm ent of AMI with beta-adrenergic receptor blockade in the clinical sett ing should be evaluated with respect to ventricular remodeling during prolonged therapy.