(Hypertension. 1999;33:811-815.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
From the Departments of Physiology and Biophysics (J.F.C., R.L.S., D.J.D., K.C., H.L.M.), Emergency Medicine (R.L.S.), and Surgery (D.J.D.), University of Mississippi Medical Center, Jackson; and the Institute of Physiology (J.-P.M.), University of Fribourg (Switzerland).
Correspondence to Joan F. Carroll, PhD, Department of Integrative Physiology, University of North Texas Health Science Center at Fort Worth, 3500 Camp Bowie Blvd, Fort Worth, TX 76107-2699. E-mail jcarroll{at}hsc.unt.edu
AbstractObesity often leads to
symptoms of cardiopulmonary congestion associated with normal
systolic but abnormal diastolic function. This
study analyzed alterations in passive diastolic
compliance in obesity using the rabbit model. New Zealand White rabbits
were fed a normal (n=8) or 10% added fat diet (n=8). After 12 weeks,
rabbits fed the high fat diet developed obesity (5.34±0.11 versus
3.68±0.04 kg, P
0.05) and left ventricular
hypertrophy (1.37±0.07 versus 0.98±0.03 g dry weight,
P
0.05). Compliance was assessed with the isolated
heart preparation by analyzing the passive end-diastolic
left ventricular pressure-volume relationship. The
pressure-volume relation was fit to an exponential function by
regression analysis; results showed that the modulus of
stiffness was greater in obese than in lean rabbits (1.21±0.16 versus
0.83±0.05, P
0.05), indicating that
diastolic compliance was reduced. Computer simulation
analyses suggested that an isolated reduction in
diastolic compliance may contribute to elevated cardiac
filling pressures and exercise intolerance. These data suggest that
diastolic compliance is reduced early in the development of
obesity and may be an important component in the reduction of cardiac
reserve in obesity.
Key Words: heart stroke volume obesity computer modeling diastolic pressure-volume relationship
This article has been cited by other articles:
![]() |
L. van Heerebeek and W. J. Paulus The dialogue between diabetes and diastole Eur J Heart Fail, January 1, 2009; 11(1): 3 - 5. [Full Text] [PDF] |
||||
![]() |
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] |
||||
![]() |
M. M. Riordan, E. P. Weiss, T. E. Meyer, A. A. Ehsani, S. B. Racette, D. T. Villareal, L. Fontana, J. O. Holloszy, and S. J. Kovacs The effects of caloric restriction- and exercise-induced weight loss on left ventricular diastolic function Am J Physiol Heart Circ Physiol, March 1, 2008; 294(3): H1174 - H1182. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. F. Carroll, W. J. Zenebe, and T. B. Strange Cardiovascular Function in a Rat Model of Diet-Induced Obesity Hypertension, July 1, 2006; 48(1): 65 - 72. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Ren, J. R. Sowers, M. F. Walsh, and R. A. Brown Reduced contractile response to insulin and IGF-I in ventricular myocytes from genetically obese Zucker rats Am J Physiol Heart Circ Physiol, October 1, 2000; 279(4): H1708 - H1714. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. W. Nickola, L. E. Wold, P. B. Colligan, G.-J. Wang, W. K. Samson, and J. Ren Leptin Attenuates Cardiac Contraction in Rat Ventricular Myocytes : Role of NO Hypertension, October 1, 2000; 36(4): 501 - 505. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. James, A. Sanbe, K. Yager, L. Martin, R. Klevitsky, and J. Robbins Genetic Manipulation of the Rabbit Heart via Transgenesis Circulation, April 11, 2000; 101(14): 1715 - 1721. [Abstract] [Full Text] [PDF] |
||||
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1999 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |