Adaptation of cardiac myosin and creatine kinase to chronic hypoxia
- contribution of anorexia and hypertension.
Pissarek, M., #, X. Bigard$, P. Mateo#, C.-Y. Guezennec$, J. A.
Hoerter#.
# Laboratoire de Cardiologie Cellulaire et Mol[theta]culaire,
INSERM U-446, Universit[theta] de Paris-Sud, Chatenay-Malabry,
France; $ D[theta]partement de Physiologie Syst[theta]mique, Centre
d'Etudes et de Recherches de M[theta]decine A[theta]rospatiale,
Bretigny sur Orge, France; (*present address: Institute of
Pharmacology and Toxicology, University Leipzig, Germany).
APStracts 3:0504H, 1996.
The effects of chronic hypobaric hypoxia (CHH, 28 days, simulated
altitude 5500m) on the cardiac expression of myosin heavy chain (MHC)
and creatine kinase (CK) was studied in rat left (LV) and right (RV)
ventricle. To separate the effects of hypoxia from its associated
perturbations anorexia and pulmonary hypertension (resulting in RV
hypertrophy), CHH animals were compared to normoxic controls (C) and
to rats restricted in food supply (pair-fed, PF). In RV the increased
proportion of (-MHC in CHH (20(3%) vs. C (7(2%, p<0.01) and
vs. PF (12(2%, p<0.05) was mainly attributed to hypertension.
In contrast the higher (-MHC of CHH (23(2%) vs. C (13(2%,
p<0.05) in LV was mainly ascribed to anorexia (PF=21(3%, ns).
A major contribution of anorexia was also evidenced in the isozymic
profile of CK: anorexia accounted for a 25% decrease mito-CK specific
activity in LV whereas hypertension partly accounts for the 3 fold
increase in BB-CK in RV. CHH specifically induced a 2 fold rise in LV
BB-CK. This suggests that both the expression of slow myosin
improving the economy of contraction and the changes in CK isozymic
profile could provide biochemical basis for the CHH resistance to
ischemia.
Received 15 July 1996; accepted in final form 5 November 1996.
APS Manuscript Number H628-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996