Difference between revisions of "Johansen 2011 Acta Physiol Scand"
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{{Publication | {{Publication | ||
|title=Johansen D, Sanden E, Hagve M, Chu X, Sundset R, Ytrehus K (2011) Heptanol triggers cardioprotection via mitochondrial mechanisms and mitochondrial potassium channel opening in rat hearts. Acta Physiol Scand 201: 435- | |title=Johansen D, Sanden E, Hagve M, Chu X, Sundset R, Ytrehus K (2011) Heptanol triggers cardioprotection via mitochondrial mechanisms and mitochondrial potassium channel opening in rat hearts. Acta Physiol Scand 201:435-44. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/21070611 PMID:21070611 ] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/21070611 PMID:21070611 ] | ||
|authors=Johansen D, Sanden E, Hagve M, Chu X, Sundset R, Ytrehus K | |authors=Johansen D, Sanden E, Hagve M, Chu X, Sundset R, Ytrehus K | ||
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{{Labeling | {{Labeling | ||
|organism=Rat | |organism=Rat | ||
|tissues=Heart | |tissues=Heart | ||
|preparations=Isolated | |preparations=Isolated mitochondria | ||
|injuries=Ischemia-reperfusion;preservation | |||
|instruments=Oxygraph-2k | |||
}} | }} | ||
Revision as of 13:16, 13 February 2015
| Johansen D, Sanden E, Hagve M, Chu X, Sundset R, Ytrehus K (2011) Heptanol triggers cardioprotection via mitochondrial mechanisms and mitochondrial potassium channel opening in rat hearts. Acta Physiol Scand 201:435-44. |
Johansen D, Sanden E, Hagve M, Chu X, Sundset R, Ytrehus K (2011) Acta Physiol Scand
Abstract: Aim: To investigate mechanisms behind heptanol (Hp)-induced infarct size reduction and in particular if protection by pre-treatment with Hp is triggered through mitochondrial mechanisms.
Methods: Langendorff perfused rat hearts, isolated mitochondria and isolated myocytes were used. Infarct size, mitochondrial respiration, time to mitochondrial permeability transition pore (MPTP) opening and AKT and glycogen synthase kinase 3 beta (GSK-3Ξ²) phosphorylation were examined.
Results: Pre-treatment with Hp reduced infarct size from 29.7 Β± 3.4% to 12.6 Β± 2.1%. Mitochondrial potassium channel blockers 5-hydroxy decanoic acid (5HD) blocking mitoK(ATP) and paxilline (PAX) blocking mitoK(Ca) abolished cardioprotective effect of Hp (Hp + 5HD 36.7 Β± 2.9% and Hp + PAX 40.2 Β± 2.8%). Hp significantly reduced respiratory control ratio in both subsarcolemmal and interfibrillar mitochondria in a dose-dependent manner (0.5-5.0 mm). The ADP oxygen ratio was also significantly reduced by Hp (2 mm). Laser scanning confocal microscopy of tetramethylrhodamine-loaded isolated rat myocytes using line scan mode showed that Hp increased time to MPTP opening. Western blot analysis showed that pre-treatment with Hp increased phosphorylation of AKT and GSK-3Ξ² before ischaemia and after 30 min of global ischaemia.
Conclusion: Pre-treatment with Hp protects the heart against ischaemia-reperfusion injury. This protection is most likely mediated via mitochondrial mechanisms which initiate a signalling cascade that converges on inhibition of opening of MPTP. β’ Keywords: cardioprotection, gap junction, heptanol, ischaemia, mitochondria, potassium channels
β’ O2k-Network Lab: NO_Tromso_Larsen TS
Labels:
Stress:Ischemia-reperfusion;preservation"Ischemia-reperfusion;preservation" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Rat Tissue;cell: Heart Preparation: Isolated mitochondria
HRR: Oxygraph-2k
