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Cardiovascular Research Advance Access [Accepted Manuscript] published online on January 25, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn017
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Adiponectin protects against myocardial ischemia/reperfusion injury via AMPK, Akt and nitric oxide

Adrian T Gonon1,, Ulrika Widegren2, Aliaksandr Bulhak1, Firoozeh Salehzadeh2, Jonas Persson3, Per-Ove Sjöquist1 and John Pernow1

1 Departments of Medicine, Unit of Cardiology, 171 77 Stockholm, Sweden
2 Departments of Molecular Medicine and Surgery, Section of Integrative Physiology, 171 77 Stockholm, Sweden
3 Departments of Danderyd University Hospital, Karolinska Institutet, 171 77 Stockholm, Sweden

Corresponding author: Adrian T. Gonon, Department of Cardiology, Karolinska University Hospital, Solna, 171 76 Stockholm, tel. +46 8 517 70 000, fax +46 8 31 10 40, e-mail: adrgon{at}ki.se

Aim: Cardiovascular disease and type 2 diabetes mellitus are associated with low plasma concentration of adiponectin. The aim of this study was to investigate whether adiponectin exerts cardioprotective effects during myocardial ischemia/reperfusion and whether this effect is related to production of nitric oxide (NO).

Method: Isolated rat hearts were subjected to 30 min of either global or local ischemia followed by 60 min reperfusion. The hearts received vehicle, adiponectin (3µg/ml), the NO-synthase inhibitor L-NNA (0.1 mM) or a combination of adiponectin and L-NNA at the onset of ischemia. Hemodynamics, infarct size and expression of endothelial NO-synthase (eNOS), AMP-activated protein kinase (AMPK) and Akt were determined.

Results: Adiponectin significantly increased left ventricular function and coronary flow during reperfusion in comparison with the vehicle group. Co-administration of L-NNA abrogated the improvement in myocardial function induced by adiponectin. Infarct size following local ischemia-reperfusion was 40±6% of the area at risk in the vehicle group. Adiponectin reduced infarct size to 19±2% (P<0.01). L-NNA did not affect infarct size per se but abolished the protective effect of adiponectin (infarct size 40±5%). Phosphorylation of eNOS Ser1177, AMPK Thr172 and Akt Ser 473 was increased in the adiponectin group (P<0.05).

Conclusion: Adiponectin protects from myocardial contractile dysfunction and limits infarct size following ischemia and reperfusion by a mechanism involving activation of AMPK and production of NO.

KEYWORDS adiponectin; nitric oxide; ischemia; reperfusion; heart

Time for primary review : 29


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