Fig. 3. Effects of opioids on cell death as assessed by propidium iodide (PI) uptake. Cardiomyocytes, equilibrated at normoxic conditions for 40 min (baseline), were subjected to infusion for 10 min of morphine or BW373U86, followed by 10 min of a drug-free period. Control cells were equilibrated at normoxic conditions for 60 min (Cont). All cells were subjected to 60 min of ischemia and 3 h of reoxygenation. Morphine (Mor) or BW373U86 significantly reduced cell death compared with controls. Treatment with naloxone (Nalo+Mor) or 7-benzylidenenaltrexone (BNTX+Mor) abolished the protection of morphine (A ). The protection of BW373U86 was abolished by diethyldithiocarbamic acid (DDC), an inhibitor for H2O2production (DDC+BW) or 5-hydroxydecanoate (5-HD+BW;B ). * P < 0.05.

Fig. 3. Effects of opioids on cell death as assessed by propidium iodide (PI) uptake. Cardiomyocytes, equilibrated at normoxic conditions for 40 min (baseline), were subjected to infusion for 10 min of morphine or BW373U86, followed by 10 min of a drug-free period. Control cells were equilibrated at normoxic conditions for 60 min (Cont). All cells were subjected to 60 min of ischemia and 3 h of reoxygenation. Morphine (Mor) or BW373U86 significantly reduced cell death compared with controls. Treatment with naloxone (Nalo+Mor) or 7-benzylidenenaltrexone (BNTX+Mor) abolished the protection of morphine (A ). The protection of BW373U86 was abolished by diethyldithiocarbamic acid (DDC), an inhibitor for H2O2production (DDC+BW) or 5-hydroxydecanoate (5-HD+BW;B ). * P < 0.05.

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