Document Detail


Energy metabolism in normal and hypertrophied right ventricle of the ferret heart.
MedLine Citation:
PMID:  9236144     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Using an isolated ferret heart preparation (Langendorff perfusion, perfusion pressure 90 mmHg), energy metabolism has been characterized in right and left ventricles from control and hypertrophied hearts. Hypertrophy was induced by pulmonary artery clipping for 30-45 days (right ventricle wall weight/body weight ratio increased by 70%). Myocardial contents of high energy phosphate compounds, glycogen and lactate, and the activities of some enzymes were biochemically measured in perfused hearts and also after ischemic arrest (30 min global ischemia). In hypertrophied right ventricles, PCr (-46%), Cr (-34%) levels, creatine kinase activity (-18%) were significantly decreased compared with control. ATP and Pi levels were not affected by hypertrophy. The adenylate energy charges were similar (0.85-0.86) in both types of heart. The activities of hexokinase (+26%), aldolase (+212%), pyruvate kinase (+14%) and glucose 6-phosphate dehydrogenase (+107%) were increased by hypertrophy. The LDH isozyme pattern was significantly changed such that LDH3 was decreased by 11%, and LDH4 and LDH5 were increased by a factor 1.4 and 2.9 respectively in hypertrophy. After 30 min of global ischemia, PCr level was decreased by 89 and 79% in control and hypertrophied ventricles respectively. ATP level was depressed by 41 in control and only by 21% in hypertrophied muscles. Altogether, the present data suggested that, in the adult ferret heart, the capacity for the ATP synthesis could be maintained during hypertrophy by the enhancement of the glycolytic pathway. The smaller decline of ATP after ischemia in hypertrophied tissue could be explained by a lower consumption of ATP in the hypertrophied compared to the control heart during the earliest period of ischemia.
Authors:
E Do; S Baudet; M Verdys; C Touzeau; F Bailly; B Lucas-Héron; M Sagniez; A Rossi; J Noireaud
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  29     ISSN:  0022-2828     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  1997 Jul 
Date Detail:
Created Date:  1997-08-21     Completed Date:  1997-08-21     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  1903-13     Citation Subset:  IM    
Affiliation:
Laboratory of Cellular & Molecular Physiopathology &, Pharmacology, CJF INSERM 96-01, Grenoble, France.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / metabolism
Age Factors
Animals
Cardiomegaly / metabolism*
Creatine Kinase / metabolism
Energy Metabolism
Ferrets
Glycolysis
Myocardium / metabolism*
Phosphates / metabolism
Phosphocreatine / metabolism
Chemical
Reg. No./Substance:
0/Phosphates; 56-65-5/Adenosine Triphosphate; 67-07-2/Phosphocreatine; EC 2.7.3.2/Creatine Kinase

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