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European Heart Journal Advance Access originally published online on January 24, 2006
European Heart Journal 2006 27(7):875-881; doi:10.1093/eurheartj/ehi751
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Oxidative modification of tropomyosin and myocardial dysfunction following coronary microembolization

Marcella Canton1, Andreas Skyschally2, Roberta Menabò1, Kerstin Boengler2, Petra Gres2, Rainer Schulz2, Michael Haude3, Raimund Erbel3, Fabio Di Lisa1 and Gerd Heusch2,*

1Department of Biochemistry, University of Padova, Italy
2Institute of Pathophysiology, University School of Medicine Essen, Hufelandstr. 55, 45122 Essen, Germany
3Department of Cardiology, University School of Medicine Essen, Essen, Germany

Received 28 October 2005; revised 21 December 2005; accepted 5 January 2006; online publish-ahead-of-print 24 January 2006.

* Corresponding author: Tel: +49 201 723 4480; fax: +49 201 723 4481. E-mail address: gerd.heusch{at}uni-essen.de

See page 764 for the editorial comment on this article (doi:10.1093/eurheartj/ehi742)

Aims We addressed a potential mechanism of myocardial dysfunction following coronary microembolization at the level of myofibrillar proteins.

Methods and results Anaesthetized pigs underwent intracoronary infusion of microspheres. After 6 h, the microembolized areas (MEA) had decreased systolic wall thickening to 38±7% of baseline and a 2.62±0.40-fold increase in the formation of disulphide cross-bridges (DCB) in tropomyosin relative to that in remote areas. The impairment in contractile function correlated inversely with DCB formation (r=–0.68; P=0.015) and was associated with increased TNF-{alpha} content. DCB formation was reflected by increased tropomyosin immunoreactivity and abolished in vitro by dithiothreitol. Ascorbic acid prevented contractile dysfunction as well as increased DCB and TNF-{alpha}. In anaesthetized dogs, 8 h after intracoronary microspheres infusion, contractile function was reduced to 8±10% of baseline and DCB in MEA was 1.48±0.12 higher than that in remote areas. In conscious dogs, 6 days after intracoronary microspheres infusion, myocardial function had returned to baseline and DCB was no longer different between remote and MEA. Again contractile function correlated inversely with DCB formation (r=–0.83; P=0.005).

Conclusion Myofibrillar protein oxidation may represent a mechanistic link between inflammation and contractile dysfunction following coronary microembolization.

Key Words: Microcirculation • Inflammation • Myocardial contraction


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