Heart failure occurs in increased oxidative stress conditions, which contribute to the progression of pathological changes. Orally or intravenously administered acetylsalicylic acid (ASA, aspirin) is typically used in human patients with acute myocardial ischemia. The study used an experimental porcine ischemia-reperfusion model to evaluate the potential cardioprotective effect of intracoronary administered ASA on myocardial ischemia-reperfusion injury. The cardioprotective effect of ASA was evaluated by measuring selected oxidative stress markers levels in infarcted and non-infarcted myocardium 14 days after the procedure, and three times in serum, before the procedure, during the reperfusion process, and after 14-day recovery. The results showed that intracoronary administrated ASA reduced the oxidative stress. The level of oxidative stress, measured with the non-enzymatic markers total antioxidant capacity (TAC), total oxidative status (TOS), and malondialdehyde (MDA), and the enzymatic markers glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione S-transferase (GST), in heart tissue was significantly higher in a control group injected with saline. The level of oxidative stress in serum, measured with TAC, TOS, oxidative stress index (OSI), and lipofuscin (LF), was also higher in the control group than in animals injected with ASA. The confirmed cardioprotective effect of intracoronary administered ASA provides the foundation for further studies on ASA intracoronary application, which may lead to the development of a new therapy for the treatment of ischemia-reperfusion complications in humans.
Keywords: acetylsalicylic acid; myocardial ischemia-reperfusion; oxidative stress markers.