Circulation, Vol 87, 1249-1257, Copyright © 1993 by American Heart Association
NM Magid, JS Borer, MS Young, DC Wallerson and C DeMonteiro
BACKGROUND. The heart adapts to the volume overload of aortic regurgitation
with dilation and hypertrophy. The development of left ventricular
hypertrophy at the protein level is a dynamic process resulting from an
imbalance between cardiac protein synthesis and degradation. The objective
of the present study was to determine in vivo the relative contributions of
cardiac protein synthesis and degradation to the progressive hypertrophy
that occurs in response to chronic aortic regurgitation and to compare
these with responses earlier in the course of this stress. METHODS AND
RESULTS. Continuous intravenous infusions of [3H]-leucine were administered
3 days and 1 month after surgical induction of aortic regurgitation and
sham operation in rabbits. Total cardiac protein and myosin heavy chain
fractional synthesis rates were obtained by analysis of plasma and protein
hydrolysate data using [14C]-dansyl chloride assays. Left ventricular
growth rates were determined from serial echocardiographic and postmortem
left ventricular weight and protein concentration measurements; protein
degradation rates were determined by subtraction of growth rates from
synthesis rates. CONCLUSIONS. In comparison with sham-operated control
rabbits, protein fractional synthesis rates were increased at 3 days but
not at 1 month after induction of aortic regurgitation Progressive cardiac
hypertrophy occurring at 1 month was caused by a decrease in protein
fractional degradation rates. An increase in protein synthesis contributes
only to the early phase of hypertrophy caused by acute aortic
regurgitation, whereas progressive eccentric hypertrophy in chronic volume
overload is due to suppression of protein degradation.
ARTICLES
Suppression of protein degradation in progressive cardiac hypertrophy of chronic aortic regurgitation
Department of Medicine, Cornell University Medical College, New York Hospital-Cornell Medical Center, NY 10021.
This article has been cited by other articles:
 |
|
 |
|
  D. W. Rodenbaugh, H. L. Collins, D. G. Nowacek, and S. E. DiCarlo Increased susceptibility to ventricular arrhythmias is associated with changes in Ca2+ regulatory proteins in paraplegic rats Am J Physiol Heart Circ Physiol, December 1, 2003; 285(6): H2605 - H2613. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. S. Borer and R. O. Bonow Contemporary Approach to Aortic and Mitral Regurgitation Circulation, November 18, 2003; 108(20): 2432 - 2438. [Full Text] [PDF]
|
|
|
|
|
|
T. Matsuo, B. A. Carabello, Y. Nagatomo, M. Koide, M. Hamawaki, M. R. Zile, and P. J. McDermott Mechanisms of cardiac hypertrophy in canine volume overload Am J Physiol Heart Circ Physiol, July 1, 1998; 275(1): H65 - H74. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. S. Borer, C. Hochreiter, E. McM. Herrold, P. Supino, M. Aschermann, D. Wencker, R. B. Devereux, M. J. Roman, M. Szulc, P. Kligfield, et al. Prediction of Indications for Valve Replacement Among Asymptomatic or Minimally Symptomatic Patients With Chronic Aortic Regurgitation and Normal Left Ventricular Performance Circulation, February 17, 1998; 97(6): 525 - 534. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. A Movsesian and R. H.G Schwinger Calcium sequestration by the sarcoplasmic reticulum in heart failure Cardiovasc Res, February 1, 1998; 37(2): 352 - 359. [Full Text] [PDF]
|
|
|
|
|
|
T. Ueyama, T. Ohkusa, Y. Hisamatsu, Y. Nakamura, T. Yamamoto, M. Yano, and M. Matsuzaki Alterations in cardiac SR Ca2+-release channels during development of heart failure in cardiomyopathic hamsters Am J Physiol Heart Circ Physiol, January 1, 1998; 274(1): H1 - H7. [Abstract] [Full Text] [PDF]
|
|