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Articles in PresS, published online ahead of print February 14, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00872.2001
Submitted on October 9, 2001
Accepted on January 29, 2002
1 Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan
2 Cardiovascular Institute, University of Pittsburgh Medical Center, Pittsburgh, PA, USA
* To whom correspondence should be addressed. E-mail: kubotat{at}cardiol.med.kyushu-u.ac.jp.
Transgenic mice with cardiac-specific overexpression of tumor necrosis factor (TNF)- (TG) develop dilated cardiomyopathy with myocardial inflammation. The purpose of this study was to investigate the role of nitric oxide (NO) in this mouse model of cardiomyopathy. Female TG and wild-type mice (WT) at the age of 10 weeks were studied. Expression and activity of inducible nitric oxide synthase (iNOS) were significantly increased in the TG myocardium, while those of endothelial NOS were not altered. Majority of the iNOS protein was isolated in the interstitial cells. A selective iNOS inhibitor ONO-1714 was used to examine the effects of iNOS induction on myocardial contractility. Echocardiography and left ventricular pressure measurements were performed. Both fractional shortening and +dP/dtmax were significantly suppressed in TG. Although ONO-1714 did not change hemodynamic parameters or contractility at baseline, it significantly improved ß-adrenergic inotropic responsiveness in TG. These results indicate that induction of iNOS may play an important role in the pathogenesis of cardiac dysfunction in this mouse model of cytokine-induced cardiomyopathy.
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