Biol. Pharm. Bull. 30(3) 460—464 (2007)

tent free radical scavenger, is currently used in the treatment of acute ischemic stroke. Its ability to prevent lipid peroxidation is comparable to that of ascorbic acid and a-tocopherol. Furthermore, it has been recently reported to confer protection against ischemia-induced neuronal damage in the neonatal rat brain. Mortality of ischemic heart diseases is significantly higher in old people than in young adults. There is very little information in the literature regarding age-related changes in myocardial function, injury, and inflammation during cerebral ischemia-reperfusion (IR) in vivo. Oxidative stress plays a critical role in IR. Reactive oxygen species (ROS) have the potential to injure cardiomyocytes, vascular cells, and endothelial cells directly, and may trigger an inflammatory cascade by inducing cytokine expression. Damage induced by ROS on intracellular and extracellular targets, such as membrane lipids, protein, and DNA clearly contributes to myocyte necrosis and/or apoptosis and organ dysfunction during myocardial IR. Normally, ROS are quickly inactivated by the antioxidative system; therefore the severity of oxidative tissue injury is determined by the balance between ROS production and intrinsic antioxidative capacity of the tissue. Aging may increase ROS production or enhance the toxic effects of ROS via impairment of antioxidative efficiency during myocardial IR. A devastating consequence of tissue reperfusion is the development of damage in organs uninvolved in the initial ischemic insult. From the standpoint of organ protection in the setting of IR, the heart is as important as the brain; because: a) the heart is a vital organ; and b) it is much less equipped in antioxidant defenses than other organs e.g. liver and intestines. In this study, we looked into the brain of IR-related myocardial damage in aged rats because this model simulates the clinical situation. Experimental data and clinical experience indicate that injury of the brain is often accompanied by secondary injury of the heart. In a previous study, we found that 45-min reperfusion of the brain after 85 min of ischemia triggers simultaneously an accumulation of protein carbonyl and mitogen-activated protein kinases (MAPKs) changes in the rat heart. In the present study, we focused on the effect of edaravone in the myocardial tissue of aged rat. We demonstrated that edaravone treatment significantly inhibits myocardial damage by regulating oxidative stress and the MAPKs pathway after cerebral IR.