| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1Division of Cardiology, Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky; and 2Department of Molecular and Cellular Physiology, 3Department of Surgery, and 4Division of Cardiology, Department of Medicine, Louisiana State University Health Sciences Center, Shreveport, Louisiana; and 5The Whitaker Cardiovascular Institute, Boston University Medical Center, Boston, Massachusetts
Submitted 11 March 2004 ; accepted in final form 19 August 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–/–) 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 = 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 1 mo. Deficiency of iNOS did not alter survival during CHF compared with wild type (35% vs. 32%, P = not significant). Furthermore, fractional shortening and cardiac output were not significantly different between wild-type (9.6 ± 2.0% and 441 ± 20 µl·min–1·g–1) and iNOS–/– (9.8 ± 1.3% and 471 ± 26 µl·min–1·g–1) mice. The extent of cardiac hypertrophy and pulmonary edema was also similar between wild-type and iNOS–/– mice. None of the indexes demonstrated any significant differences between iNOS–/– 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
This article has been cited by other articles:
|
|
 |
|
  W. D. Gilson, F. H. Epstein, Z. Yang, Y. Xu, K.-M. R. Prasad, M.-C. Toufektsian, V. E. Laubach, and B. A. French Borderzone Contractile Dysfunction Is Transiently Attenuated and Left Ventricular Structural Remodeling Is Markedly Reduced Following Reperfused Myocardial Infarction in Inducible Nitric Oxide Synthase Knockout Mice J. Am. Coll. Cardiol., October 30, 2007; 50(18): 1799 - 1807. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Zhang, X. Xu, X. Hu, E. D. van Deel, G. Zhu, and Y. Chen Inducible Nitric Oxide Synthase Deficiency Protects the Heart From Systolic Overload-Induced Ventricular Hypertrophy and Congestive Heart Failure Circ. Res., April 13, 2007; 100(7): 1089 - 1098. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Pacher, J. S. Beckman, and L. Liaudet Nitric Oxide and Peroxynitrite in Health and Disease Physiol Rev, January 1, 2007; 87(1): 315 - 424. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. J. M. Greer, D. P. Ware, and D. J. Lefer Myocardial infarction and heart failure in the db/db diabetic mouse Am J Physiol Heart Circ Physiol, January 1, 2006; 290(1): H146 - H153. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y.-H. Liu, O. A. Carretero, O. H. Cingolani, T.-D. Liao, Y. Sun, J. Xu, L. Y. Li, P. J. Pagano, J. J. Yang, and X.-P. Yang Role of inducible nitric oxide synthase in cardiac function and remodeling in mice with heart failure due to myocardial infarction Am J Physiol Heart Circ Physiol, December 1, 2005; 289(6): H2616 - H2623. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Sun, O. A. Carretero, J. Xu, N.-E. Rhaleb, F. Wang, C. Lin, J. J. Yang, P. J. Pagano, and X.-P. Yang Lack of Inducible NO Synthase Reduces Oxidative Stress and Enhances Cardiac Response to Isoproterenol in Mice With Deoxycorticosterone Acetate-Salt Hypertension Hypertension, December 1, 2005; 46(6): 1355 - 1361. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
