Pretreatment of rabbit isolated hearts with iloprost at 27 or 270 nM improved myocardial functional recovery, reduced CPK and glutathione release, and attenuated oxidative stress during reperfusion.
Does iloprost pretreatment improve functional recovery and attenuate oxidative stress in rabbit isolated hearts during ischaemia and reperfusion?
Iloprost pretreatment attenuates oxidative stress and improves functional recovery in isolated rabbit hearts subjected to ischaemia-reperfusion injury.
Reperfusion of rabbit isolated hearts after 60 min of ischaemia resulted in poor recovery of mechanical function, release of creatine phosphokinase (CPK) and of reduced (GSH) and oxidized (GSSG) glutathione, reduction of mitochondrial superoxide dismutase (Mn SOD) activity and of tissue GSH/GSSG ratio with a shift of cellular thiol redox state toward oxidation, suggesting the occurrence of oxidative stress. 2. Pretreatment of the isolated heart with the stable prostacyclin analogue (iloprost) at 27 or 270 nM, but not at 2.7 nM, improved the functional recovery of the myocardium, reduced CPK, GSH and GSSG release, maintained Mn SOD activity and attenuated the occurrence of oxidative stress. 3. This effect of iloprost cannot be explained by a decreased demand or an enhanced delivery of oxygen during ischaemia or by a direct effect on glutathione peroxidase and reductase activity.
Ferrari et al. (Sun,) conducted a other in Ischaemia and reperfusion injury. Iloprost (ZK 36374) vs. Untreated ischaemia/reperfusion was evaluated on Functional recovery, CPK release, GSH and GSSG release, Mn SOD activity, and oxidative stress. Pretreatment of rabbit isolated hearts with iloprost at 27 or 270 nM improved myocardial functional recovery, reduced CPK and glutathione release, and attenuated oxidative stress during reperfusion.
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