Tolerance of acute hypercapnic acidosis by the European eel (Anguilla anguilla)

Abstract.

European eels (Anguilla anguilla) were exposed sequentially to partial pressures of CO₂ in the water (PwCO₂) of 5, 10, 20, 40, 60 then 80 mm Hg (equivalent to 0.66–10.5 kPa), for 30 min at each level. This caused a profound drop in arterial plasma pH, from 7.9 to below 7.2, an increase in arterial PCO₂ from 3.0 mm Hg to 44 mm Hg, and a progressive decline in arterial blood O₂ content (caO₂) from 10.0% to 1.97% volume. Gill ventilation rate increased significantly at water PwCO₂s of 10, 20 and 40 mm Hg, followed by a decline at PwCO₂s of 60 and 80 mm Hg, due to periodic breathing. Mean opercular pressure amplitude increased steadily throughout hypercapnic exposure and was significantly elevated at a PwCO₂ of 80 mm Hg. Hypercapnia caused a tachycardia between PwCO₂s of 5 mmHg and 10 mm Hg, followed by a progressive decline in heart rate. Cardiac output (CO) remained unchanged throughout, as a consequence of a significant increase in stroke volume at PwCO₂s of 40, 60 and 80 mm Hg. The eels maintained O₂ uptake at routine normocapnic levels throughout hypercapnic exposure. A comparison of the rates of blood O₂ delivery (calculated from CO and caO₂) against O₂ consumption at PwCO₂s of 60 mm Hg and 80 mm Hg indicated that a portion of O₂ uptake was due to cutaneous respiration. Thus, the European eel's exceptional tolerance of acute hypercapnia is probably a consequence of the tolerance of its heart to acidosis and hypoxia, and a contribution to O₂ uptake from cutaneous respiration.