Vitamin A is beneficial in counteracting free radical damage, therefore the present study is designed to investigate the effect of vitamin A against isoproterenol-induced myocardial infarction in rats. Male Wistar rats were divided into three groups, namely a normal control group, an isoproterenol group (150 mg/kg, s.c.), and a vitamin A treatment (4,500 IU/kg/d, orally) group. Vitamin A-treated rats demonstrated significant reduction in ST-segment (p<0.001) and infarct sizes (p<0.05) when compared with the isoproterenol group of rats, suggesting that vitamin A markedly attenuated myocardial injury. Vitamin A treatment resulted in a significant decrease in the serum level of troponin I (p<0.001), creatinine kinase-MB (p<0.01), creatine kinase (p<0.05), lactate dehydrogenase (p<0.05), aspartate aminotransferase (p<0.01) and alanine aminotransferase (p<0.01). Vitamin A treatment resulted in a significant decrease in malondialdehyde (p<0.001), and significant increases were observed in reduced glutathione (p<0.01), superoxide dismutase (p<0.05) and catalase (p<0.001). Vitamin A treatment resulted in a significantly increased level of Na⁺-K⁺ ATPase (p<0.05) and Mg²⁺-ATPase (p<0.01) and a significant reduction of Ca²⁺ ATPase (p<0.01). Vitamin A treatment also demonstrated a significantly decreased level of C-reactive protein (p<0.05) and myeloperoxidase activity (p<0.01). In conclusion, vitamin A attenuated the myocardial infarction and prevention was shown via membrane stabilization, reduction in oxidative stress, and prevention of neutrophil infiltration.