Effects of hydromorphone postconditioning on ischemia-reperfusion injury in isolated rat hearts and mitochondial permeability transition pore

To investigate the effects of hydromorphone postconditioning on ischemia/reperfusion injury in isolated rat hearts and mitochondial permeability transition pore (mPTP). Male SD rat hearts were harvested and then perfused in a Langendorff apparatus with K-H solution saturate. Rat hearts were randomly assigned into 4 groups (n = 10): Control group (group C), ischemia reperfusion group (group I/R), Hydromorphone postconditioning group (group H) and hydromorphone + Lonidamine postconditioning group (group HL). Group C was perfused continuously for 120 min; the rest groups were perfused for 30 min and treated by 30 min of ischemia followed by 60 min reperfusion to establish I/R injury model. Group H was received 10 min postconditioning treatment with 0.3 mu mol/L hydromorphone after 30 min ischemia, group HL was received 0.3 mu mol/L hydromorphone and 30 mu mol/L Lonidamine for postconditioning at the same time. Compared with group C, LVDP, CF, +dp/dtmax and the fluorescence intensity of cardiomyocytes were significantly decreased in the rest groups, while LVEDP, LDH, CK-MB, Tn-T, NAD+, infarct size were significantly increased (P < 0.05). Compared with group H, LVDP, CF, +/- dp/dtmax, HR and the fluorescence intensity of cardiomyocytes were significantly decreased in the group HL and group I/R, while LVEDP, LDH, CK-MB, Tn-T, NAD+, infarct size were significantly increased. There was no significant difference between group HL and group I/R except LDH (P = 0.012) and HR (P = 0.034). Hydromorphone can attenuate the I/R injury in isolated rat hearts, and 30 mu mol/L Lonidamine (mPTP opener) can significantly abolished the effect of hydromorphone on myocardial protection.