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Am J Physiol Heart Circ Physiol (January 30, 2003). doi:10.1152/ajpheart.00888.2002
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Submitted on October 15, 2002
Accepted on January 24, 2003

Increased myocardial oxygen consumption by TNF{alpha} is mediated by a sphingosine-signaling pathway

Ulrich D. Hofmann1, Erik Domeier2, Stefan Frantz1, Martin Laser1, Barbara Weckler1, Peter Kuhlencordt1, Stefan Heuer1, Boris Keweloh2, Georg Ertl1, and Andreas W Bonz1*

1 Department of Cardiology, Medizinische Universitaetsklinik Wuerzburg, Wuerzburg, Germany
2 Department of Cardiology, University of Goettingen, Goettingen, Germany

* To whom correspondence should be addressed. E-mail: bonz_a{at}klinik.uni-wuerzburg.de.

The present study investigates the effect of tumor necrosis factor {alpha}(TNF-{alpha}) on myocardial energy metabolism as estimated by myocardial oxygen consumption (MVO2). MVO2 of electrically stimulated isolated trabeculae of right ventricular Wistar rat myocardium were analyzed using a clark-type oxygen probe. Following initial data collection in the absence of TNF-{alpha}, measurements were repeated after TNF-{alpha} stimulation. In separate experiments pretreatment with the NO synthase inhibitor N(G)nitro-L-arginine methyl ester (L-NAME) or the ceramidase inhibitor n-oleoylethanolamine (NOE) was done to investigate NO/sphingosine related effects. TNF-{alpha} impaired myocardial economy at increasing stimulation frequencies without altering baseline MVO2. Incubation with TNF-{alpha} in the presence of L-NAME further impaired myocardial economy. NOE preincubation abrogated the TNF-{alpha} effect on myocardial economy. Moreover, the negative inotropic effect of TNF-{alpha} was observed in NOE, but not in L-NAME pretreated muscle fibers. Exogenous sphingosine mimicked the TNF-{alpha} effect on mechanics and energetics. We conclude, that TNF-{alpha} impairs the economy of chemo-mechanical energy transduction primarily through a sphingosine-mediated pathway.




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