HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 290/1/H146    most recent 00583.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (17) Citing Articles via Google Scholar Google Scholar Articles by Greer, J. J. M. Articles by Lefer, D. J. Search for Related Content PubMed PubMed Citation Articles by Greer, J. J. M. Articles by Lefer, D. J.

Myocardial infarction and heart failure in the db/db diabetic mouse

¹Department of Molecular and Cellular Physiology and ²Department of Surgery, Louisiana State University Health Sciences Center, Shreveport, Louisiana

Submitted 2 June 2005 ; accepted in final form 1 August 2005

Clinical studies have reported that the incidence and severity of myocardial infarction is significantly greater in diabetics compared with nondiabetics after correction for all other risk factors. The majority of studies investigating the pathophysiology of myocardial ischemia-reperfusion injury have focused on otherwise healthy animals. At present, there is a paucity of experimental investigations on the pathophysiology of heart failure in diabetic animals. We hypothesized that the severity of myocardial reperfusion injury and the development of congestive heart failure would be markedly enhanced in the db/db diabetic mouse. Accordingly, we studied the effects of varying durations of in vivo myocardial ischemia and reperfusion on the incidence of heart failure in db/db diabetic mice. Nondiabetic and db/db diabetic mice (10 wk of age) were subjected to 30, 45, or 60 min of left coronary artery occlusion and 28 days of reperfusion. Survival at 24 h of reperfusion was 100% in nondiabetic mice subjected to 30 min of myocardial ischemia and 88% in nondiabetic mice subjected to 45 min of myocardial ischemia. In contrast, survival was 53% in db/db diabetic mice subjected to 30 min of myocardial ischemia and 44% in db/db mice after 45 min of myocardial ischemia. Prolonged survival in nondiabetic mice was not significantly attenuated when compared during the 28-day follow-up period with all groups experiencing >90% survival. Prolonged survival was significantly decreased in db/db mice after both 30 and 45 min of myocardial ischemia compared with sham controls. Furthermore, we observed a significant degree or left ventricular dilatation, cardiac hypertrophy, and cardiac contractile dysfunction in db/db mice subjected to 45 min of myocardial ischemia and 28 days reperfusion. In nondiabetic mice subjected to 45 min of myocardial ischemia, we failed to observe any changes in left ventricular dimensions or fractional shortening. These studies provide a feasible experimental model system for the investigation of heart failure secondary to acute myocardial infarction in the db/db diabetic mouse.

diabetes mellitus; ischemia; reperfusion; left ventricular dimension; hypertrophy; contractility

This article has been cited by other articles:

				E. D. Abel, S. E. Litwin, and G. Sweeney Cardiac Remodeling in Obesity Physiol Rev, April 1, 2008; 88(2): 389 - 419. [Abstract] [Full Text] [PDF]

				I. Lekli, G. Szabo, B. Juhasz, S. Das, M. Das, E. Varga, L. Szendrei, R. Gesztelyi, J. Varadi, I. Bak, et al. Protective mechanisms of resveratrol against ischemia-reperfusion-induced damage in hearts obtained from Zucker obese rats: the role of GLUT-4 and endothelin Am J Physiol Heart Circ Physiol, February 1, 2008; 294(2): H859 - H866. [Abstract] [Full Text] [PDF]

				K. R. McGaffin, C.-K. Sun, J. J. Rager, L. C. Romano, B. Zou, M. A. Mathier, R. M. O'Doherty, C. F. McTiernan, and C. P. O'Donnell Leptin signalling reduces the severity of cardiac dysfunction and remodelling after chronic ischaemic injury Cardiovasc Res, January 1, 2008; 77(1): 54 - 63. [Abstract] [Full Text] [PDF]

				Z. Lu, Y.-P. Jiang, X.-H. Xu, L. M. Ballou, I. S. Cohen, and R. Z. Lin Decreased L-Type Ca2+ Current in Cardiac Myocytes of Type 1 Diabetic Akita Mice Due to Reduced Phosphatidylinositol 3-Kinase Signaling Diabetes, November 1, 2007; 56(11): 2780 - 2789. [Abstract] [Full Text] [PDF]

				M. P. Chandler, E. E. Morgan, T. A. McElfresh, T. A. Kung, J. H. Rennison, B. D. Hoit, and M. E. Young Heart failure progression is accelerated following myocardial infarction in type 2 diabetic rats Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1609 - H1616. [Abstract] [Full Text] [PDF]

				S. Boudina and E. D. Abel Diabetic Cardiomyopathy Revisited Circulation, June 26, 2007; 115(25): 3213 - 3223. [Abstract] [Full Text] [PDF]

				J. W. Elrod, J. J. M. Greer, and D. J. Lefer Sildenafil-mediated acute cardioprotection is independent of the NO/cGMP pathway Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H342 - H347. [Abstract] [Full Text] [PDF]

				G. D. Thakker, N. G. Frangogiannis, M. Bujak, P. Zymek, J. W. Gaubatz, A. K. Reddy, G. Taffet, L. H. Michael, M. L. Entman, and C. M. Ballantyne Effects of diet-induced obesity on inflammation and remodeling after myocardial infarction Am J Physiol Heart Circ Physiol, November 1, 2006; 291(5): H2504 - H2514. [Abstract] [Full Text] [PDF]

				D. An and B. Rodrigues Role of changes in cardiac metabolism in development of diabetic cardiomyopathy Am J Physiol Heart Circ Physiol, October 1, 2006; 291(4): H1489 - H1506. [Abstract] [Full Text] [PDF]

				P. H. McNulty Metabolic responsiveness to insulin in the diabetic heart Am J Physiol Heart Circ Physiol, May 1, 2006; 290(5): H1749 - H1751. [Full Text] [PDF]