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

European eels (Anguilla anguilla) were exposed sequentially to partial pressures of CO2 in the water (PwCO(2)) 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 O-2 content (caO(2)) from 10.0% to 1.97% volume. Gill ventilation rate increased significantly at water PwCO(2)s of 10, 20 and 40 mm Hg, followed by a decline at PwCO(2)s 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 PwCO(2) of 80 mm Hg. Hypercapnia caused a tachycardia between PwCO(2)s 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 PwCO(2)s of 40, 60 and 80 mm Hg. The eels maintained O-2 uptake at routine normocapnic levels throughout hypercapnic exposure. A comparison of the rates of blood O-2 delivery (calculated from CO and caO(2)) against O-2 consumption at PwCO(2)s of 60 mm Hg and 80 mm Hg indicated that a portion of O-2 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 O-2 uptake from cutaneous respiration.