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1 Cardiology, University of Louisville, Louisville, KY, USA
2 Physiology, LSU Health Sciences Center, Shreveport, LA, USA
3 Surgery, LSU Health Sciences Center, Shreveport, LA, USA
4 Whitaker Cardiovascular Institute, Boston University Medical Center, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: dlefer{at}lsuhsc.edu.
Inducible nitric oxide synthase (iNOS) has been implicated in the pathophysiology of congestive heart failure (CHF). Given the extensive evidence supporting this concept, we hypothesized that deficiency (-/-) of iNOS would attenuate the severity of congestive heart failure in mice. Mice were subjected to permanent occlusion (MI) of the proximal left anterior descending coronary artery to produce CHF. Cardiac function was assessed in vivo using echocardiography and ultraminiature ventricular pressure catheters. Sham wild-type (n = 17), sham iNOS-/- (n = 8), MI wild-type (n = 56), and MI iNOS-/- (n = 48) mice were subjected to MI (or sham MI) and followed for one month. Deficiency of iNOS did not alter survival during congestive heart failure compared to wild-type (35% vs. 32%, p = NS). Furthermore, fractional shortening and cardiac output were not significantly different between wild-type (9.6 ± 2.0 % and 441 ± 20 µL/min/g) and iNOS-/- (9.8 ± 1.3 % and 471 ± 26 µL/min/g) mice. The extent of cardiac hypertrophy and pulmonary edema was also similar between wild-type and iNOS-/- mice. None of the indices demonstrated any significant differences between iNOS-/- mice and wild-type mice subjected to myocardial infarction. These findings indicate that deficiency of iNOS does not significantly affect severe congestive heart failure in mice following myocardial infarction.
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