ROLE OF NITRIC OXIDE IN CARDIAC PERFORMANCE DURING EXPERIMENTAL ISCHEMIC CARDIAC ARREST AND REPERFUSION

Abstract

Background: Re-perfusion strategies are the current standard therapy for acute myocardial infarction, despite the spectrum of re-perfusionassociated pathologies that may contribute to irreversible myocardial injury. Aim of the work: The aim of present study is to clarify the alterations in intrinsic cardiac functions in response to cardiac ischemic arrest followed by re-perfusion in isolated hearts perfused with nitric oxide (NO) donor, Larginine, or NO inhibitor, Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME), to shed light on the possible role of NO in re-perfusion process. Materials and Methods: Cardiac activities of hearts isolated from Adult albino rats of both sexes were studied on Langendorff preparation under basal conditions and during 30 min re-perfusion following 30 min of total global ischemia. Rats were randomly allocated into three groups; control and L-arginine or L-NAME infused heart groups. Both L-arginine and LNAMEwere infused over 20 min during the baseline activity before induction of total global ischemia. Thereafter, cardiac tissue levels of malondialdhyde, catalase and nitrite were assessed. Results: Compared to the control, both L arginine and L-NAME infused hearts showed increased basal chronotropy and myocardial flow rate. Significantly depressed basal inotropic state was only observed in L-arginine group. The three studied groups demonstrated significant deterioration in the inotropic activity and compromised myocardial flow rate during the whole period of reperfusion. L-arginine infused hearts demonstrated depressed inotropy and chronotropy, weak systolic and diastolic functions with compromised myocardial flow at early 5 min of reperfusion, yet with significantly higher myocardial flow rate % recovery by the end ofreperfusion (82.7% ±3.01 in L-arginine vs. 56.4% ± 2.32 in control and 62.6% ±2.17 in L-NAME). The chronotropic activity was maintained in both the control and L-NAME infused hearts. Cardiac tissue NO showed the highest level in L-arginine group and the lowest level in L-NAME one. Both catalase and MDA were insignificantly changed among the three studied groups. Conclusion: Reducing NO availability by L-NAME revealed mild impact on the ischemia re-perfusion induced contractile dysfunction. Excess NO worsens cardiac performance at early re-perfusion. However, it may have potentially protective effect by acquiring higher the myocardial flow rate during the reperfusion.