ArticleCanadian journal of anaesthesia = Journal canadien d'anesthesie2010
Morphine induces preconditioning via activation of mitochondrial K(Ca) channels.
Article in Canadian journal of anaesthesia = Journal canadien d'anesthesie, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 20 citations in OpenAlex.
- SK channel-mediated metabolic escape to glycolysis inhibits ferroptosis and supports stress resistance in C. elegans.Cell death & disease · 2020Article
- Impact of Anesthetics on Cardioprotection Induced by Pharmacological Preconditioning.Journal of clinical medicine · 2019Article
- Morphine-Induced Preconditioning: Involvement of Protein Kinase A and Mitochondrial Permeability Transition Pore.PloS one · 2016Article
- Impact of Mitochondrial Ca2+-Sensitive Potassium (mBKCa) Channels in Sildenafil-Induced Cardioprotection in Rats.PloS one · 2015Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
purposeMitochondrial 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.
methodsIsolated 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.
resultsInfarct 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).
conclusionCardioprotection by morphine-induced preconditioning is mediated by activation of mK(Ca) channels.
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