AJP - Heart Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Heart Circ Physiol 258: H51-H56, 1990;
0363-6135/90 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Litwin, S. E.
Right arrow Articles by Bressler, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Litwin, S. E.
Right arrow Articles by Bressler, R.

AJP - Heart and Circulatory Physiology, Vol 258, Issue 1 51-H56, Copyright © 1990 by American Physiological Society


ARTICLES

Chronic inhibition of fatty acid oxidation: new model of diastolic dysfunction

S. E. Litwin, T. E. Raya, R. G. Gay, J. B. Bedotto, J. J. Bahl, P. G. Anderson, S. Goldman and R. Bressler
Department of Internal Medicine, Veterans Administration Medical Center, Tucson 85723.

This study was designed to determine the changes in the heart that result from inhibition of long-chain fatty acid oxidation with 2-tetradecylglycidic acid (TDGA). Male Sprague-Dawley rats (n = 64) were treated with TDGA (20 mg.kg-1.day-1) or a comparable volume of vehicle by gavage feeding for 7 or 21 days. In conscious rats TDGA produced no changes in heart rate, left ventricular systolic or end-diastolic pressures, left ventricular pressure development (dP/dt), or the time constant of left ventricular relaxation. Left ventricular developed pressure was not changed at 21 days. TDGA increased left ventricular weight, left ventricular weight-to-body weight ratio, and total heart weight-to-body weight ratio. Left ventricular endocardial and epicardial myocyte volumes were increased by 53 and 65%, respectively. Myocardial triglyceride content was increased threefold. Left ventricular chamber stiffness constants between end-diastolic pressures of 0 and 30 mmHg were increased, and left ventricular end-diastolic volumes at operating end-diastolic pressures were decreased at both 7 and 21 days. The myocardial stiffness constant was also increased at 7 and 21 days. Thus inhibition of long-chain fatty acid oxidation with TDGA increased left ventricular mass and altered left ventricular chamber and muscle stiffness without changing left ventricular relaxation or systolic function. We conclude that inhibition of long-chain fatty acid oxidation produced an unusual model of left ventricular hypertrophy and diastolic dysfunction characterized by abnormalities of passive-elastic properties but preserved relaxation.


This article has been cited by other articles:


Home page
DiabetesHome page
R. L. Dobbins, L. S. Szczepaniak, B. Bentley, V. Esser, J. Myhill, and J. D. McGarry
Prolonged Inhibition of Muscle Carnitine Palmitoyltransferase-1 Promotes Intramyocellular Lipid Accumulation and Insulin Resistance in Rats
Diabetes, January 1, 2001; 50(1): 123 - 130.
[Abstract] [Full Text]


Home page
CirculationHome page
Y. Jamshidi, H. E. Montgomery, H.-W. Hense, S. G. Myerson, I. P. Torra, B. Staels, M. J. World, A. Doering, J. Erdmann, C. Hengstenberg, et al.
Peroxisome Proliferator-Activated Receptor {alpha} Gene Regulates Left Ventricular Growth in Response to Exercise and Hypertension
Circulation, February 26, 2002; 105(8): 950 - 955.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online