No abstract

. Deficiency of iNOS does not attenuate severe congestive heart failure in mice. Am J Physiol Heart Circ Physiol 288: H365-H370, 2005. First published August 19, 2004; doi:10.1152/ajpheart.00245.2004.-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 iNOS deficiency (iNOS Ϫ/Ϫ ) would attenuate the severity of CHF in mice. Mice were subjected to permanent occlusion [myocardial infarction (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 ϭ 17), sham iNOS Ϫ/Ϫ (n ϭ 8), MI wild-type (n ϭ 56), and MI iNOS Ϫ/Ϫ (n ϭ 48) mice were subjected to MI (or sham MI) and followed for 1 mo. Deficiency of iNOS did not alter survival during CHF compared with wild type (35% vs. 32%, P ϭ not significant). Furthermore, fractional shortening and cardiac output were not significantly different between wild-type (9.6 Ϯ 2.0% and 441 Ϯ 20 l ⅐ min Ϫ1 ⅐ g Ϫ1 ) and iNOS Ϫ/Ϫ (9.8 Ϯ 1.3% and 471 Ϯ 26 l ⅐ min Ϫ1 ⅐ g Ϫ1 ) mice. The extent of cardiac hypertrophy and pulmonary edema was also similar between wild-type and iNOS Ϫ/Ϫ mice. None of the indexes demonstrated any significant differences between iNOS Ϫ/Ϫ and wild-type mice subjected to MI. These findings indicate that deficiency of iNOS does not significantly affect severe CHF in mice after MI. myocardial infarction; nitric oxide; physiology; inducible nitric oxide synthase