Effects of Rosiglitazone on prevention of left ventricular remodeling after acute myocardial infarction in rats

【Objectives】To assess the effects of peroxisome proliferator activated receptor-γ activators Rosiglitazone on the prevention of left ventricular remodeling after acute myocardial infarction (AMI) in rats. 【Methods】AMI were conducted by ligating left coronary artery in female SD rats. 24 hours after the procedure, 118 survival rats were randomly divided into AMI controls (n = 60) and Rosiglitazone treatment group (n = 58), with the drug therapy initiated immediately. Shamoperated rats (n = 30) were randomly selected to serve as noninfarction controls. Then, the rats in each of the 3 groups were further divided, and observed or treated for 1, 2 or 4 weeks respectively. After the completion of treatment, hemodynamic studies were performed. The heart of rats were fixed and analyzed pathologically. Exclusive the dead rats and the hearts with the MI size 35% or 50%, complete experimental data were obtained in 103 rats. The number of rats for each treatment period in each group was 9~12. 【Results】There was no significant difference in MI size between AMI controls and Rosiglitazone group for each of the 3 treatment periods (42%~48%, all P 0.05). Compared with shamoperated rats, left ventricular (LV)end diastolic pressure (LVEDP) and LV absolute weight (LVAW) and relative weight (LVRW)were significantly increased in AMI controls at 1, 2 and 4 weeks after AMI (P 0.05~0.001), with LVEDP elevated significantly more at 4 weeks than at 1 and 2 weeks after AMI (all P 0.01); whereas ±dp/ dt and its corrected value by LV systolic pressure (±dp/dt/LVSP) were all significantly reduced only at 4 weeks after AMI (all P 0.001). Compared with AMI controls, LVEDP was significantly reduced at all 1, 2 and 4 weeks after AMI in Rosiglitazone group (P 0.05~0.001), with LVAW and LVRW bothsignificantly reduced (P 0.05~0.001) and 2 dp/dt and ±dp/dt/LVSP all significantly raised only at 4 weeks after AMI (P 0.05~0.01). 【Conclusion】Rosiglitazone can effectively prevent left ventricular remodeling and improve its systolic and diastolic functions after AMI in rat.