| Summary: | Eels reared intensively in recirculated water can experience chronic hypercapnia from accumulation of metabolic CO 2 , with water CO 2 partial pressures ( P w,CO 2 ) exceeding 30 mmHg, far above that hitherto considered normal for fish (1 to 3 mmHg). The effects on eels of acute and chronic hypercapnia were investigated. Eels ( n = 6) were anaesthetised (0.05 % MS-222 in water), cannulated in the dorsal aorta for withdrawal of blood samples and in the operculum for measurement of gill ventilation rate ( f G ) and pressure amplitude ( P OP ). A flow cuff placed on the ventral aorta measured cardiac output (CO). Eels were recovered for 48 h in respirometer chambers provided with a flow of normocapnic water. Instantaneous O 2 uptake was measured every 10 min with an automated system. All data are reported as means ± S.E.M., means compared by ANOVA, significance attributed at P < 0.05. Acute exposure to progressive hypercapnia (20 min at P w,CO 2 values of 10, 20, 40, 60 and 80 mmHg) caused a linear increase in arterial P CO 2 ( P a,CO 2 ) from 3.5 ± 0.4 mmHg in normocapnia to 44.9 ± 2.6 at P w,CO 2 = 80 mmHg, coupled to respective declines in arterial pH (pH a ) from 7.86 ± 0.02 to 7.16 ± 0.04 and in arterial total O 2 content ( c a, O 2 ) from 9.6 ± 0.7 to 2.0 ± 0.5 vol%. There was a significant increase in f G and P OP at P w,CO 2 values of 10, 20, 40 mmHg, then a decline in f G but further increase in P OP at P w,CO 2 = 60 and 80 mmHg. Despite the severe acidosis and hypoxaemia, there were no significant effects on CO or O 2 uptake. Eels exposed for 3 months to chronic hypercapnia ( P w,CO 2 values of control, 15, 30 or 45 mmHg) were anaesthetised, cannulated and recovered as described above, at the appropriate P w,CO 2 . In all groups, P a,CO 2 was about 3 mmHg above P w,CO 2 , and hypercapnic eels exhibited a marked accumulation of plasma bicarbonate, from 12.8 ± 1.5 mmol l -1 in controls ( n = 6) to 72.5 ± 4.1 at P w,CO 2 = 45 mmHg ( n = 4). The bicarbonate accumulation buffered the effects of hypercapnia on pH a and c a, O 2 , as compared with the acute exposure. Nonetheless, in the eels at P w,CO 2 = 45 mmHg, pH a was 7.57 ± 0.04 and c a, O 2 5.5 ± 2.2 vol%, significantly lower than in the control animals, where pH a was 7.89 ± 0.04 and c a, O 2 11.6 ± 1.5 vol%. Exercise performance was studied in a swimming respirometer. Stepwise increases in swimming speed caused similar, exponential increases in O 2 uptake in all groups, with no differences in tailbeat frequencies, aerobic scope or maximum sustainable swimming speed. The results indicate that the eel is extremely tolerant of hypercapnic acidosis. Acute, severe acidosis and hypoxaemia had no effect on CO or whole animal O 2 uptake; chronic acidosis and hypoxaemia had no effect on the ability to increase O 2 uptake and perform muscular work during exercise.
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