Substrate mobilization and hormonal changes in rainbow trout (Oncorhynchus mykiss, L.) and common carp (Cyprinus carpio, L.) during deep hypoxia and subsequent recovery

• Published in: Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology Biochemical, systemic, and environmental physiology, 1996-11, Vol.166 (7), p.443-452
• Main Authors: Raaij, M. T. M., Thillart, G. E. E. J. M., Vianen, G. J., Pit, D. S. S., Balm, P. H. M., Steffens, A. B.
• Format: Article
• Language: English
• Subjects: Cyprinus carpio; Freshwater; Oncorhynchus mykiss
• ISSN: 0174-1578; 1432-136X
• DOI: 10.1007/BF02337889

Common carp (Cyprinus carpio) (at 20 degree C) and rainbow trout (Oncorhynchus mykiss) (at 15 degree C) were fitted with an indwelling cannula in the dorsal aorta. The fish were exposed to a controlled decline of water pO sub(2) followed by 90 min deep hypoxia at 0.3 kPa (carp) or 4.8 kPa (trout). Thereafter, normoxic recovery was monitored in both species for 48 h. At regular intervals blood samples were analysed for glucose, lactate, free fatty acids, adrenaline, noradrenaline and cortisol. The oxygen restriction was maximal in both species and resulted in a significant increase of plasma lactate levels. In carp, adrenaline, noradrenaline and cortisol levels increased to 2, 50, and 753 ng/ml respectively during anoxia, whereas in trout these hormones increased to 12, 8 and 735 ng/ml respectively during hypoxia. In hypoxic trout, the plasma levels of glucose (3 mol/l) were increased modestly whereas levels of free fatty acids (0.25 mmol/l) were decreased to 0.15 mmol/l. In carp, however, a marked and prolonged hyperglycaemia (from 5 to 10 mmol/l) and a significant continuous depression of plasma levels of free fatty acids (from 0.4 to 0.2 mmol/l) were observed indicating a difference in metabolic organization. It is suggested that hyperglycaemia is likely to be the result of hepatic glycogenolysis, stimulated by circulating catecholamines and a stimulation of gluconeogenesis by cortisol during recovery. The mechanism for the decline of plasma levels of free fatty acids is most probably a reduction of lipolytic activity, which appears to be an adaptation to hypoxia.