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- W2047164463 abstract "The aim of the study was to examine the cardioprotective effect of morphine and Delta 2 opioid d-Ala2-Leu5 enkephalin (DADLE) administered, at early reoxygenation, in isolated human myocardium exposed to hypoxia–reoxygenation. Then, we tested the involvement of mitochondrial permeability transition pore in morphine and DADLE-induced postconditioning. Human right atrial trabeculae were obtained during cardiac surgery (coronary artery bypass and aortic valve replacement). Isometrically contracting isolated human right atrial trabeculae were exposed to 30-min hypoxia and 60-min reoxygenation (control group). In treatment groups, morphine 0.5 μmol, DADLE 10 nmol, DADLE 50 nmol and DADLE 100 nmol were administered during the first 15 min of reoxygenation. In two additional groups, morphine and DADLE 100 nmol were administered in the presence of atractyloside 50 μmol, the mitochondrial permeability transition pore opener. The force of contraction at the end of 60-min reoxygenation period (FoC 60 expressed as % of baseline) was compared (mean ± standard deviation) between the groups by an analysis of variance. Morphine (FoC 60 : 81 ± 9% of baseline), DADLE 50 nmol (FoC 60 : 76 ± 11% of baseline) and DADLE 100 nmol (FoC 60 : 81 ± 4% of baseline) increased significantly ( P < 0.001) the FoC 60 as compared with the control group (FoC 60 : 53 ± 3% of baseline). DADLE 10 nmol did not modify the FoC 60 (50 ± 9% of baseline; P = 0.60 versus control group). The enhanced recovery of FoC 60 induced by morphine and DADLE 100 nmol were abolished in the presence of atractyloside (FoC 60 : respectively 57 ± 6% and 44 ± 7% of baseline; P < 0.001). In conclusion, the administration of morphine and DADLE, in early reoxygenation period, protected human myocardium, in vitro, against hypoxia–reoxygenation injury, at least in part, by the inhibition of mitochondrial permeability transition pore opening." @default.
- W2047164463 created "2016-06-24" @default.
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- W2047164463 date "2013-04-01" @default.
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- W2047164463 title "[d-Ala2,d-Leu5]-enkephalin (DADLE) and morphine-induced postconditioning by inhibition of mitochondrial permeability transition pore, in human myocardium" @default.
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- W2047164463 doi "https://doi.org/10.1177/1535370212474602" @default.
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