Resveratrol (RES; trans-3,5,4'-trihydroxystilbene) has been shown to improve 
health and slow the progression of disease in various models. Several 
cardioprotective mechanisms have been identified including antioxidant, 
anti-inflammatory, and antifibrotic actions. Each of these actions is thought to 
have the ability to attenuate the pathophysiology underlying the deleterious 
cardiac structural remodeling that results from acute myocardial infarction 
(MI). Therefore, we evaluated the effect of resveratrol treatment on the 
progression of cardiac remodeling after MI. Four groups of rats (sham, n = 6; 
sham + RES, n = 21; MI, n = 26; MI + RES, n = 24) were treated for 13 weeks, 
starting 7 days before ligation of the left anterior descending coronary artery. 
Serial transthoracic echocardiography revealed that resveratrol had no effect on 
MI-induced left-ventricular and left-atrial dilatation or reduction in 
left-ventricular fractional shortening. Consistent with these findings, 
resveratrol did not improve the deterioration of hemodynamic function or reduce 
infarct size at 12 weeks post-MI. Resveratrol-treated animals did, however, show 
preserved cardiac contractile reserve in response to dobutamine administration. 
Radioligand binding revealed that MI reduced beta-adrenergic receptor density. 
Resveratrol administration increased beta-adrenoceptor density, so that 
resveratrol-treated MI rats had beta-adrenoceptor densities similar to normal 
rats. Real-time reverse transcription-polymerase chain reaction revealed that 
MI-induced changes in sarcoplasmic reticulum Ca2+-ATPase 2 and transforming 
growth factor beta-1 expression were unaltered by resveratrol, whereas 
MI-induced increases in atrial natriuretic factor (ANF) and connective tissue 
growth factor (CTGF) expression were attenuated. Resveratrol treatment does not 
improve cardiac remodeling and global hemodynamic function post-MI but does 
preserve contractile reserve and attenuate ANF and CTGF up-regulation.