Skeletal muscle [beta]-adrenoreceptors and phosphate metabolism
abnormalities in heart failure in rats.
Chati, Zuka[diaeresis]i, Christophe Michel, Jean Marie Escanye, Paul
Michel Mertes, Christophe Ribuot, Daniel Canet, Fa[diaeresis]iez
Zannad.
Department of Cardiology and Pharmacology, Biophysics Laboratory,
and Experimental Surgery Laboratory, University of Henri
Poincar[acute]e, Nancy, France
APStracts 3:0187H, 1996.
In order to investigate the mechanisms leading to skeletal muscle
metabolic abnormalities in chronic heart failure (CHF), we studied
phosphate metabolism and skeletal muscle [beta]-adrenoreceptors
([beta]-AR) in rats 12-14 wk after coronary ligation (CL). We
performed 31P magnetic resonance spectroscopy (31P MRS) in the
gastrocnemius muscle during motor activity produced by electrical
stimulation (5HZ). The initial slope of Phosphocreatine (PCr)
depletion was higher in the CL rats compared to sham operated rats (
Pi/PCr/time: 0.211+/-0.045 vs. 0.113+/-0.029; p<0.05). During
recovery, both PCr resynthesis rate and maximal rate of oxidative ATP
synthesis (Vmax. ) were reduced 3-fold in the CL rats compared with
controls (11+/-2 vs. 37+/-7 mmol/l/min.; p<0.04 and 20+/-3 vs.
79+/-18 mmol/l/min.; p<0.03 respectively). There were no
significant differences either for the skeletal muscle density (13+/
-6 vs. 15+/-3 fM/mg) or for the affinity ( 0.244+/-0.149 vs. 0.246+/
-0.146 nM) of [beta]-AR between the two groups. This study showed that
although in moderate CHF skeletal muscle metabolic abnormalities can
be demonstrated, these changes could not be explained by skeletal
muscle [beta]-adrenergic receptors alterations in this experimental
model.
Received 8 November 1995; accepted in final form 18 April 1996.
APS Manuscript Number H1046-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 8 May 96