Cardioprotective effect of the alcoholic extract of Terminalia arjuna bark in an in vivo model of myocardial ischemic reperfusion injury

The present study was designed to investigate the effects of chronic administration of the alcoholic extract of Terminalia arjuna (TAAE) bark on isoproterenol induced myocardial injury. The TAAE was administered orally to Wistar albino rats (150-200 g) in three different doses, by gastric gavage [3.4 mg/kg: (TI), 6.75 mg/kg: (T2) and 9.75 mg/kg: (T3)] 6 days/week for 4 weeks. At the end of this period, all the animals, except the normal untreated rats that served as the control group, were administered isoproterenol (ISO) 85 mg/kg, S.C., for two consecutive days to induce in vivo myocardial injury. After 48 hours rats were anaesthetized with anaesthetic ether, then sacrificed and the hearts were harvested for biochemical and histological studies. A significant rise in myocardial thiobarbituric acid reactive substances (TBARS) and loss of reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (suggestive of increased oxidative stress) occurred in the hearts subjected to in vivo myocardial ischemic reperfusion injury. The 6.75 mg/kg TAAE treatment group (baseline) shows a significant increase in myocardial TBARS as well as endogenous antioxidants (GSH, SOD, and catalase), but not in the other treatment groups. In in vivo ischemic reperfusion injury of the TAAE treated rats there was a significant decrease in TBARS in all the groups. In 6.75 mg/kg treatment group, a significant rise in the levels of GSH, SOD and catalase were observed, and it shows better recovery profile than the other groups subjected to in vivo ischemic reperfusion injury. In histological studies, all the groups, except the isoproterenol treated group, showed preserved myocardium. The present study demonstrates that the 6.75 mg/kg TAAE augments endogenous antioxidant compounds of the rat heart and also prevents the myocardium from isoproterenol induced myocardial ischemic reperfusion injury. (C) 2003 Elsevier Inc. All rights reserved.