caa a22 4500 477118542 CHVBK 20180405111629.0 cr unu---uuuuu 170330e19960301xx s 000 0 eng 10.1007/BF00239322 doi (NATIONALLICENCE)springer-10.1007/BF00239322 Postischemic injury in isolated rat hearts is not aggravated by prior depletion of myocardial glutathione [Elektronische Daten] [Robert Verbunt, Willem Van Dockum, E. Lars Bastiaanse, Janneke Egas, Amoud Van der Laarse] The aim of this study was to test the hypothesis that a decreased myocardial concentration of reduced glutathione (GSH) during ischemia renders the myocardium more susceptible to injury by reactive oxygen species generated during early reperfusion. To this end, rats were pretreated with L-buthionine-S,R-sulfoximine (2 mmol/kg), which depleted myocardial GSH by 55%. Isolated buffer-perfused hearts were subjected to 30 min of either hypothermic or normothermic no-flow ischemia followed by reperfusion. Prior depletion of myocardial GSH did not lead to oxidative stress during reperfusion, as myocardial concentration of glutathione disulfide (GSSG) was not increased after 5 and 30 min of reperfusion. In addition, prior depletion of GSH did not exacerbate myocardial enzyme release, nor did it impair the recoveries of tissue ATP, coronary flow rate and left ventricular developed pressure during reperfusion after either hypothermic or normothermic ischemia. Even administration of the prooxidant cumene hydroperoxide (20 μM) to postischemic GSH-depleted hearts during the first 10 min of reperfusion did not aggravate postischemic injury, although this prooxidant load induced oxidative stress, as indicated by an increased myocardial concentration of GSSG. These results do not support the hypothesis that a reduced myocardial concentration of GSH during ischemia increases the susceptibility to injury mediated by reactive oxygen species generated during reperfusion. Apparently, myocardial tissue possesses a large excess of GSH compared to the quantity of reactive oxygen species generated upon reperfusion. (Mol Cell Biochem 156: 79-85, 1996) Kluwer Academic Publishers, 1996 ischemia nationallicence reperfusion nationallicence oxidative stress nationallicence glutathione nationallicence buthionine sulfoximine nationallicence Verbunt Robert Department of Cardiology, University Hospital Leiden, Leiden, The Netherlands aut Van Dockum Willem Department of Cardiology, University Hospital Leiden, Leiden, The Netherlands aut Lars Bastiaanse E. Department of Cardiology, University Hospital Leiden, Leiden, The Netherlands aut Egas Janneke Department of Cardiology, University Hospital Leiden, Leiden, The Netherlands aut Van der Laarse Amoud Department of Cardiology, University Hospital Leiden, Leiden, The Netherlands aut Molecular and Cellular Biochemistry Kluwer Academic Publishers 156/1(1996-03-01), 79-85 0300-8177 156:1<79 1996 156 11010 https://doi.org/10.1007/BF00239322 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00239322 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Verbunt Robert Department of Cardiology, University Hospital Leiden, Leiden, The Netherlands aut NATIONALLICENCE 700 1- Van Dockum Willem Department of Cardiology, University Hospital Leiden, Leiden, The Netherlands aut NATIONALLICENCE 700 1- Lars Bastiaanse E. Department of Cardiology, University Hospital Leiden, Leiden, The Netherlands aut NATIONALLICENCE 700 1- Egas Janneke Department of Cardiology, University Hospital Leiden, Leiden, The Netherlands aut NATIONALLICENCE 700 1- Van der Laarse Amoud Department of Cardiology, University Hospital Leiden, Leiden, The Netherlands aut NATIONALLICENCE 773 0- Molecular and Cellular Biochemistry Kluwer Academic Publishers 156/1(1996-03-01), 79-85 0300-8177 156:1<79 1996 156 11010 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer