title: Energy metabolism in normal and hypertrophied right ventricle of the ferret heart.
abstract: 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.affiliation: Laboratory of Cellular & Molecular Physiopathology &, Pharmacology, CJF INSERM 96-01, Grenoble, France.
authors.forename: E
authors.initials: E
authors.lastname: Do
authors.forename: S
authors.initials: S
authors.lastname: Baudet
authors.forename: M
authors.initials: M
authors.lastname: Verdys
authors.forename: C
authors.initials: C
authors.lastname: Touzeau
authors.forename: F
authors.initials: F
authors.lastname: Bailly
authors.forename: B
authors.initials: B
authors.lastname: Lucas-Héron
authors.forename: M
authors.initials: M
authors.lastname: Sagniez
authors.forename: A
authors.initials: A
authors.lastname: Rossi
authors.forename: J
authors.initials: J
authors.lastname: Noireaud
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000367:Age Factors; D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism*; D003402:Creatine Kinase / Q000378:metabolism; D004734:Energy Metabolism; D005289:Ferrets; D006019:Glycolysis; D009206:Myocardium / Q000378:metabolism*; D010710:Phosphates / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism
chemical_list: D010710:Phosphates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D003402:Creatine Kinase