Abstract

Background Recent studies have demonstrated that PPARγ ligands have anti-inflammatory effect which is involved in ventricular remodeling. So we hypothesized that PPARγ ligand may have beneficial effects on post-infarct ventricular remodeling. Methods Experimental myocardial infarction (MI) was induced in SD rats by ligation of the left coronary artery. Twenty-four hours after surgery, survival rats were randomly divided into MI group and Rosiglitazone (MI + Ros) group which would take rosiglitazone 3 mg/kg day for 8 weeks. After 8 weeks treatment, left ventricular hemodynamics were measured and organs were weighed. Myocardial collagen analysis was determined in Van Gieson staining by quantitative morphometry. Myocardial angiotensin II and aldosterone were detected by radioimmunoassay. Myocardial AT1 and AT2 mRNA expression were determined by RT-PCR. Results Only 1 rat in MI group died of anesthesia at the 8th week. Rosiglitazone treatment could improve left ventricular ± d p/d t max, collagen volume fraction and perivascular circumferential area; reduce lung/body mass ratio and liver/body mass ratio; inhibit myocardial angiotensin II and aldosterone; and had no significant effects on myocardial AT1 and AT2 mRNA. Plasma insulin and blood glucose were comparable between two groups. Conclusions PPARγ ligand has neutral effect on mortality and beneficial effect on post-infarct ventricular remodeling, partly by suppressing myocardial angiotensin II and aldosterone, irrespective of plasma insulin and blood glucose level.

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