| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Cardiovascular Research Group, Temple University School of Medicine, Philadelphia, Pennsylvania 19107; and 2 Division of Kinesiology and Health, 3 Department of Animal Science, University of Wyoming, Laramie, Wyoming 82071
To date, no study has assessed the degree of similarity between left ventricular (LV) reverse remodeling and atrophic remodeling. Stable LV hypertrophy was induced by creation of an arteriovenous fistula (AVF) in Lewis rats (32 days). LV unloading was induced by heterotopic transplantation of normal (NL-HT) and/or hypertrophic (AVF-HT) hearts (7 days). We compared indexes of remodeling in AVF, NL-HT, and AVF-HT groups with those of normal controls. LV unloading induced decreases in cardiomyocyte size in NL-HT and AVF-HT hearts. NL-HT and AVF-HT LV were both characterized by relative increases in collagen concentration that were largely a reflection of decreases in myocyte volume. NL-HT and AVF-HT LV were associated with similar increases in matrix metalloproteinase (MMP-2 and -9) zymographic activity, without change in the abundance of the tissue inhibitors of the MMPs. In contrast, AVF-HT, but not NL-HT, was associated with a dramatic increase in collagen cross-linking. Our findings suggest an overall similarity in the response of the normal and hypertrophic LV to surgical unloading. However, the dramatic increase in collagen cross-linking after just 1 wk of unloading suggests a potential difference in the dynamics of collagen metabolism between the two models. Further studies will be required to determine the precise molecular mechanisms responsible for these differences in extracellular matrix regulation. However, with respect to these and related issues, heterotopic transplantation of hypertrophied hearts will be a useful small animal model for defining mechanisms of myocyte-matrix interactions during decreased loading conditions.
myocardial atrophy; reverse remodeling; extracellular matrix; volume overload
This article has been cited by other articles:
|
|
 |
|
  T. A. Dorfman, B. D. Rosen, M. A. Perhonen, T. Tillery, R. McColl, R. M. Peshock, and B. D. Levine Diastolic suction is impaired by bed rest: MRI tagging studies of diastolic untwisting J Appl Physiol, April 1, 2008; 104(4): 1037 - 1044. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. G. Spinale Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function Physiol Rev, October 1, 2007; 87(4): 1285 - 1342. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. A. Dorfman, B. D. Levine, T. Tillery, R. M. Peshock, J. L. Hastings, S. M. Schneider, B. R. Macias, G. Biolo, and A. R. Hargens Cardiac atrophy in women following bed rest J Appl Physiol, July 1, 2007; 103(1): 8 - 16. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Suzuki, T.-S. Li, A. Mikamo, M. Takahashi, M. Ohshima, M. Kubo, H. Ito, and K. Hamano The reduction of hemodynamic loading assists self-regeneration of the injured heart by increasing cell proliferation, inhibiting cell apoptosis, and inducing stem-cell recruitment J. Thorac. Cardiovasc. Surg., April 1, 2007; 133(4): 1051 - 1058. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. V. Pancheva, V. S. Panchev, A. V. Suvandjieva, and B. D. Levine Lower body negative pressure vs. lower body positive pressure to prevent cardiac atrophy after bed rest and spaceflight. What caused the controversy? J Appl Physiol, March 1, 2006; 100(3): 1090 - 1090. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Klotz, R. F. Foronjy, M. L. Dickstein, A. Gu, I. M. Garrelds, A.H. Jan Danser, M. C. Oz, J. D'Armiento, and D. Burkhoff Mechanical Unloading During Left Ventricular Assist Device Support Increases Left Ventricular Collagen Cross-Linking and Myocardial Stiffness Circulation, July 19, 2005; 112(3): 364 - 374. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
