Key result
Morphine preconditioning significantly reduced myocardial infarct size to 23% of the area at risk compared to 45% in controls, an effect that was abolished by the mKCa channel blocker paxilline.
Why the study?
Does morphine preconditioning reduce infarct size in isolated rat hearts?
Does morphine preconditioning reduce infarct size in isolated rat hearts?
Morphine induces cardioprotection against ischemia-reperfusion injury via activation of mitochondrial calcium-sensitive potassium channels, similar to ischemic preconditioning.
Supports further mechanistic studies of opioid preconditioning; leaves open translation to human ischemia-reperfusion injury.
PURPOSE: Mitochondrial calcium sensitive potassium (mK(Ca)) channels are involved in cardioprotection induced by ischemic preconditioning. In the present study we investigated whether morphine-induced preconditioning also involves activation of mK(Ca) channels. METHODS: Isolated rat hearts (six groups; each n = 8) underwent global ischemia for 30 min followed by a 60-min reperfusion. Control animals were not further treated. Morphine preconditioning (MPC) was initiated by two five-minute cycles of morphine 1 microM infusion with one five-minute washout and one final ten-minute washout period before ischemia. The mK(Ca) blocker, paxilline 1 microM, was administered, with and without morphine administration (MPC + Pax and Pax). As a positive control, we added an ischemic preconditioning group (IPC) alone and combined with paxilline (IPC + Pax). At the end of reperfusion, infarct sizes were determined by triphenyltetrazoliumchloride staining. RESULTS: Infarct size was (mean +/- SD) 45 +/- 9% of the area at risk in the Control group. The infarct size was less in the morphine or ischemic preconditioning groups (MPC: 23 +/- 8%, IPC: 20 +/- 5%; each P < 0.05 vs Control). Infarct size reduction was abolished by paxilline (MPC + Pax: 37 +/- 7%, P < 0.05 vs MPC and IPC + Pax: 36 +/- 6%, P < 0.05 vs IPC), whereas paxilline alone had no effect (Pax: 46 +/- 7%, not significantly different from Control). CONCLUSION: Cardioprotection by morphine-induced preconditioning is mediated by activation of mK(Ca) channels.
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Fräßdorf et al. (2010) studied Myocardial ischemia/reperfusion injury (n=48). Morphine vs. Control (no treatment) was evaluated on Infarct size as a percentage of the area at risk (p=<0.05). Morphine preconditioning significantly reduced myocardial infarct size to 23% of the area at risk compared to 45% in controls, an effect that was abolished by the mKCa channel blocker paxilline.
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