Tolerance of chronic hypercapnia by the European eel Anguilla anguilla.

European eels were exposed for 6 weeks to water CO(2) partial pressures (P(CO)(2)) from ambient (approx. 0.8 mmHg), through 15+/-1 mmHg and 30+/-1 mmHg to 45+/-1 mmHg in water with a total hardness of 240 mg l(-1) as CaCO(3), pH 8.2, at 23+/-1 degrees C. Arterial plasma P(CO)(2) equilibrated at approximately 2 mmHg above water P(CO)(2) in all groups, and plasma bicarbonate accumulated up to 72 mmol l(-1) in the group at a water P(CO)(2) of 45 mmHg. This was associated with an equimolar loss of plasma Cl(-), which declined to 71 mmol l(-1) at the highest water P(CO)(2). Despite this, extracellular acid-base compensation was incomplete; all hypercapnic groups tolerated chronic extracellular acidoses and reductions in arterial blood O(2) content (Ca(O)(2)), of progressive severity with increasing P(CO)(2). 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 Ca(O)(2) was reduced by approximately 50% at the highest P(CO)(2), 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 O(2) requirements of routine and active metabolism despite profound hypoxaemia.

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

European eels ( Anguilla anguilla) were exposed sequentially to partial pressures of CO(2) 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 PCO(2) 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.

Fish as model in pharmacological and biological research.

Fish represent the oldest and most diverse classes of vertebrates, comprising around the 48% of the known member species in the subphylum Vertebrata. There are many scientific fields that use fish as models in research, including respiratory and cardiovascular research, cell culture, ecotoxicology, ageing, pharmacological and genetic studies.