Johansen 2011 Acta Physiol Scand: Difference between revisions

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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: 435-444.
|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
|instruments=Oxygraph-2k
|injuries=Ischemia-Reperfusion; Preservation
|organism=Rat
|organism=Rat
|tissues=Heart
|tissues=Heart
|preparations=Isolated Mitochondria
|preparations=Isolated mitochondria
|injuries=Ischemia-reperfusion;preservation
|instruments=Oxygraph-2k
}}
}}

Revision as of 13:16, 13 February 2015

Publications in the MiPMap
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.

ยป PMID:21070611

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-3ฮฒ) phosphorylation were examined.

Results: Pre-treatment with Hp reduced infarct size from 29.7 ยฑ 3.4% to 12.6 ยฑ 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 ยฑ 2.9% and Hp + PAX 40.2 ยฑ 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-3ฮฒ 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. โ€ข Keywords: cardioprotection, gap junction, heptanol, ischaemia, mitochondria, potassium channels

โ€ข 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 


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