| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1Experimental Cardiology Laboratory, Baker Heart Research Institute, and Alfred Heart Centre, Alfred Hospital, and 2Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia
Submitted 18 August 2004 ; accepted in final form 13 January 2005
As a prelude to investigating the mechanism of regression of pressure overload-induced left ventricular (LV) hypertrophy (LVH), we studied the time course for the development and subsequent regression of LVH as well as accompanying alterations in cardiac function, histology, and gene expression. Mice were subjected to aortic banding for 4 or 8 wk to establish LVH, and regression was initiated by release of aortic banding for 6 wk. Progressive increase in LV mass and gradual chamber dilatation and dysfunction occurred after aortic banding. LVH was also associated with myocyte enlargement, interstitial fibrosis, and enhanced expression of atrial natriuretic peptide, collagen I, collagen III, and matrix metalloproteinase-2 but suppressed expression of 
-myosin heavy chain and sarcoplasmic reticulum Ca2+-ATPase. Aortic debanding completely or partially reversed LVH, chamber dilatation and dysfunction, myocyte size, interstitial fibrosis, and gene expression pattern, each with a distinct time course. The extent of LVH regression was dependent on the duration of pressure overload, evidenced by the fact that restoration of LV structure and function was complete in animals subjected to 4 wk of aortic banding but incomplete in animals subjected to 8 wk of aortic banding. In conclusion, LVH regression comprises a variety of morphological, functional, and genetic components that show distinct time courses. A longer period of pressure overload is associated with a slower rate of LVH regression.
aortic banding; cardiac function/remodeling; model
This article has been cited by other articles:
|
|
 |
|
  W. E. Stansfield, P. C. Charles, R.-h. Tang, M. Rojas, R. Bhati, N. C. Moss, C. Patterson, and C. H. Selzman Regression of pressure-induced left ventricular hypertrophy is characterized by a distinct gene expression profile J. Thorac. Cardiovasc. Surg., January 1, 2009; 137(1): 232 - 238. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Yang, Y. Ma, W. Han, J. Li, Y. Xiang, F. Liu, X. Ma, J. Zhang, Z. Fu, Y.-D. Su, et al. Age-related differences in postinfarct left ventricular rupture and remodeling Am J Physiol Heart Circ Physiol, April 1, 2008; 294(4): H1815 - H1822. [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]
|
|
|
|
 |
|
 D. K. Yang, B. Y. Choi, Y.-H. Lee, Y.-G. Kim, M.-C. Cho, S.-E. Hong, D. H. Kim, R. J. Hajjar, and W. J. Park Gene profiling during regression of pressure overload-induced cardiac hypertrophy Physiol Genomics, June 19, 2007; 30(1): 1 - 7. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. H. Kumbar, A. VanBergen, C. Ocampo, S. Muangmingsuk, A. J. Griffin, and M. Gupta Adapter molecule DOC-2 is differentially expressed in pressure and volume overload hypertrophy and inhibits collagen synthesis in cardiac fibroblasts J Appl Physiol, May 1, 2007; 102(5): 2024 - 2032. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. J. Barrick, M. Rojas, R. Schoonhoven, S. S. Smyth, and D. W. Threadgill Cardiac response to pressure overload in 129S1/SvImJ and C57BL/6J mice: temporal- and background-dependent development of concentric left ventricular hypertrophy Am J Physiol Heart Circ Physiol, May 1, 2007; 292(5): H2119 - H2130. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
