Energy metabolism in normal and hypertrophied right ventricle of the ferret heart

被引:22
作者
Do, E
Baudet, S
Verdys, M
Touzeau, C
Bailly, F
LucasHeron, B
Sagniez, M
Rossi, A
Noireaud, J
机构
[1] HOP LAENNEC, INSERM, CJF 9601, LAB CELLULAR & MOL PHYSIOPATHOL & PHARMACOL, F-44035 NANTES, FRANCE
[2] HOP LAENNEC, INSERM, BIOCHEM LAB, F-44035 NANTES, FRANCE
[3] UFR MED, PHYSIOL LAB, F-44035 NANTES, FRANCE
[4] UNIV GRENOBLE 1, LAB BIOENERGET, F-38041 GRENOBLE, FRANCE
关键词
metabolism; ischemia; hypertrophy; ferret;
D O I
10.1006/jmcc.1997.0429
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
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 LDH, was decreased by 11%, and LDH, and LDH, 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 central 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. (C) 1997 Academic Press Limited.
引用
收藏
页码:1903 / 1913
页数:11
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