Tolerance of chronic hypercapnia by the European eel Anguilla anguilla

• Published in: Journal of Experimental Biology
• Main Authors: D. J. McKenzie, E. W. Taylor, C. L. Bolis, J. F. Steffensen, M. Piccolella, A.Z. Dalla Valle
• Other Authors: D.J. McKenzie, E.W. Taylor, C.L. Boli, J.F. Steffensen
• Format: Article in Journal/Newspaper
• Language: English
• Published: The Company of Biologists 2003
• Subjects: Acid-base balance; Aerobic scope; Anguilla anguilla; European eel; Hypercapnia; Hypoxia; Metabolic rate; Stre; Swimming performance; Settore BIO/13 - Biologia Applicata
• Online Access: http://hdl.handle.net/2434/173083; https://doi.org/10.1242/jeb.00352

European eels were exposed for 6 weeks to water CO2 partial pressures (PCO·) from ambient (approx.0.8·mmHg), through 15±1·mmHg and 30±1·mmHg to 45±1·mmHg in water with a total hardness of240·mg·l–1 as CaCO3, pH 8.2, at 23±1°C. Arterial plasma PCO· equilibrated at approximately 2·mmHg above water PCO· in all groups, and plasma bicarbonate accumulated up to 72·mmol·l–1 in the group at a water PCO· of 45·mmHg. This was associated with an equimolar loss of plasma Cl–, which declined to 71·mmol·l–1 at the highest water PCO·. Despite this, extracellular acid–base compensation was incomplete; all hypercapnic groups tolerated chronic extracellular acidoses and reductions in arterial blood O2 content (CaO·), of progressive severity with increasing PCO·. All hypercapnic eels, however, regulated the intracellular pH of heart and white muscle to the same levels as normocapnic animals. Hypercapnia had no effect on such indicators of stress as plasma catecholamine or cortisol levels, plasma osmolality or standard metabolic rate. Furthermore, although CaO· was reduced by approximately 50% at the highest PCO·, there was no effect of hypercapnia on the eels’ tolerance of hypoxia, aerobic metabolic scope or sustained swimming performance. The results indicate that, at the levels tested, chronic hypercapnia was not a physiological stress for the eel, which can tolerate extracellular acidosis and extremely low Cl– levels while compensating tissue intracellular pH, and which can meet the O2 requirements of routine and active metabolism despite profound hypoxaemia.