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Acute myocardial ischaemia induces specific alterations of ventricular mitochondrial function in experimental pigs
Service de Physiologie Clinique et des Explorations Fonctionnelles, Département de Physiologie, Faculté de Médecine, Strasbourg, France; Département de Physiologie, Faculté de Médecine, Strasbourg, France .
Service de Physiologie Clinique et des Explorations Fonctionnelles, Département de Physiologie, Faculté de Médecine, Strasbourg, France .ORCID iD: 0000-0002-8071-4745
Service de Physiologie Clinique et des Explorations Fonctionnelles, Département de Physiologie, Faculté de Médecine, Strasbourg, France .
Service de Physiologie Clinique et des Explorations Fonctionnelles, Département de Physiologie, Faculté de Médecine, Strasbourg, France .
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2005 (English)In: Acta Physiologica Scandinavica, ISSN 0001-6772, E-ISSN 1365-201X, Vol. 185, no 1, 25-32 p.Article in journal (Refereed) Published
Abstract [en]

Aims: As cardiac metabolic flexibility is crucial, this study examined whether acute ischaemia can induce specific qualitative alterations of the mitochondrial metabolic pathways as well as energy transfer systems.

Methods: Left descending coronary artery ligation was performed after sternotomy in eight pigs and the heart was excised after 45 min of ischaemia. Maximal O2 uptake (V(max), micromol O2 min(-1) g(-1) dry weight) of saponin-skinned myofibres were measured from ischaemic and non-ischaemic area of ventricular myocardium.

Results: V(max) decreased by approximately 20% in ischaemic myocardium with both glutamate-malate (18.1 +/- 1.3 vs. 22.1 +/- 1.7 in control, P < 0.05) and pyruvate substrates (19.3 +/- 1.0 vs. 23.3 +/- 2.0 in control, P < 0.05) whereas no difference was observed with palmitoyl carnitine (15.6 +/- 1.8 vs. 16.6 +/- 0.9 in control). The K(m) of mitochondrial respiration for ADP decreased in ischaemic heart by 24% (679 +/- 79 vs. 899 +/- 84 microm of ADP in control, P < 0.05). Moreover, the mitochondrial creatine kinase efficacy (K(m) without creatine/K(m) with creatine), representative of the coupling of oxidative phosphorylation process with the mitochondrial creatine kinase, was reduced in ischaemic heart (11.6 +/- 2.5 in ischaemic vs. 18.0 +/- 2.2 in control, P < 0.05).

Conclusions: These findings argue for specific mitochondrial impairments at the level of pyruvate oxidation and creatine kinase channelling system after an acute period of in vivo ischaemia, whereas the lipid mitochondrial oxidation pathway seems to be preserved. Such a loss of metabolic flexibility following acute ischaemia could become an early feature of metabolic dysregulation of the heart.

Place, publisher, year, edition, pages
Oxon, United Kingdom: Blackwell Publishing, 2005. Vol. 185, no 1, 25-32 p.
Keyword [en]
Creatine kinase, fatty acid, ischaemia, mitochondria, myocardial infarction, substrate oxidation
National Category
Medical and Health Sciences Sport and Fitness Sciences
Research subject
Sports Science
Identifiers
URN: urn:nbn:se:oru:diva-43579DOI: 10.1111/j.1365-201X.2005.01458.xISI: 000231853900004PubMedID: 16128694Scopus ID: 2-s2.0-24144479789OAI: oai:DiVA.org:oru-43579DiVA: diva2:794994
Available from: 2015-03-13 Created: 2015-03-13 Last updated: 2017-10-17Bibliographically approved

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