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 | ||
|year=2011 | |year=2011 | ||
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'''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. | '''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. | ||
|keywords= | |keywords=Cardioprotection, Gap junction, Heptanol, Ischaemia, Mitochondria, Potassium channels | ||
|mipnetlab= | |mipnetlab=NO Tromsoe Larsen TS | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|organism=Rat | |||
|tissues=Heart | |||
|preparations=Isolated mitochondria | |||
|injuries=Ischemia-reperfusion | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} | ||
Latest revision as of 17:07, 19 February 2018
| 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 Tromsoe Larsen TS
Labels:
Stress:Ischemia-reperfusion Organism: Rat Tissue;cell: Heart Preparation: Isolated mitochondria
HRR: Oxygraph-2k
