Attenuation of oxidant damage in the postconditioned heart involves non-enzymatic response and partial catalytic protection

Experimental Physiology
Francisco ArreguínCecilia Zazueta

Abstract

Oxidant stress, among other effectors, is implicated in the sequel of myocardial reperfusion injury. It is generally accepted that maintaining the balance between oxidant and antioxidant signalling within the cell provides protection against reperfusion damage. The cardioprotective strategy of postconditioning (PC) reduces reperfusion injury through complex mechanisms; however, the contribution of the antioxidant system has not been fully investigated. In this study, isolated rat hearts were subjected to PC after 30 min global ischaemia, and then to 5 min (IR5) or 60 min of reperfusion (IR60). Postconditioning significantly increased the left ventricular developed pressure and the double product (heart rate × left ventricular developed pressure) for both early (PC5) and prolonged reperfusion (PC60, PC before 60 min of reperfusion). Necrotic tissue diminished to 10.8% in PC60 hearts, compared with 49% of infarct size measured in IR60 hearts (P < 0.05 versus IR60). Also, protein carbonylation and malondialdehyde levels decreased and were correlated with a significant augmentation in CuZn superoxide dismutase activity (P < 0.05, PC60 versus IR60) and increased glutathione redox state (GSH:GSSG ratio; P < 0.05, PC60 versus IR60). D...Continue Reading

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Citations

Jul 6, 2014·Free Radical Biology & Medicine·Mabel Buelna-ChontalCecilia Zazueta
Sep 12, 2016·The American Journal of Emergency Medicine·Vincent J MaseThomas J Walters
Jul 19, 2018·American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons·Maria N SanzSarah L Longnus
Apr 22, 2018·Liver Transplantation : Official Publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society·Cecilia ZazuetaFrancisco Correa

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