ENERGY-METABOLISM IN NORMAL AND HYPERTROPHIED RIGHT VENTRICLE OF THE FERRET HEART

Citation
E. Do et al., ENERGY-METABOLISM IN NORMAL AND HYPERTROPHIED RIGHT VENTRICLE OF THE FERRET HEART, Journal of Molecular and Cellular Cardiology, 29(7), 1997, pp. 1903-1913
Citations number
46
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
00222828
Volume
29
Issue
7
Year of publication
1997
Pages
1903 - 1913
Database
ISI
SICI code
0022-2828(1997)29:7<1903:EINAHR>2.0.ZU;2-6
Abstract
Using an isolated ferret heart preparation (Langendorff perfusion, per fusion pressure 90 mmHg), energy metabolism has been characterized in right and left ventricles from control and hypertrophied hearts, Hyper trophy 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 perfuse d hearts and also after ischemic arrest (30 min global ischemia). In h ypertrophied right ventricles, PCr (-46%), Cr (-34%) levels, creatine kinase activity (-18%) were significantly decreased compared with cont rol, 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 a ctivities of hexokinase (+26%), aldolase (+212%), pyruvate kinase (+14 %) and glucose 6-phosphate dehydrogenase (+107%) were increased by hyp ertrophy. The LDH isozyme pattern was significantly changed such that LDH, was decreased by 11%, and LDH, and LDH, were increased by a facto r 1.4 and 2.9 respectively in hypertrophy, After 30 min of global isch emia, PCr level was decreased by 89 and 79% in central and hypertrophi ed ventricles respectively. ATP level was depressed by 41 in control a nd only by 21% in hypertrophied muscles, Altogether; the present data suggested that, in the adult ferret heart, the capacity for the ATP sy nthesis could be maintained during hypertrophy by the enhancement of t he glycolytic pathway, The smaller decline of ATP after ischemia in hy pertrophied tissue could be explained by a lower consumption of ATP in the hypertrophied compared to the control heart during the earliest p eriod of ischemia. (C) 1997 Academic Press Limited.