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Tolerance of chronic hypercapnia by the European eel Anguilla anguilla

D. J. McKenzie1,*, M. Piccolella2, A. Z. Dalla Valle1,2, E. W. Taylor1, C. L. Bolis2 and J. F. Steffensen3

1 School of Biosciences, University of Birmingham, Birmingham, B15 2TT, UK
2 Department of Pharmacological Sciences, Via Balzaretti, 9, University of Milan, 20133 Milan, Italy
3 Marine Biological Laboratory, University of Copenhagen, Strandpromenaden 5, DK-3000 Helsingør, Denmark



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Fig. 1. A pH–HCO3 Davenport diagram describing (black symbols) the blood acid–base status of eels exposed for at least 6 weeks to water CO2 partial pressures (PwCO2) of approx. 0.8 mmHg (ambient control), 15±1 mmHg, 30±1 mmHg or 45±1 mmHg (1 mmHg=approx. 0.01316 kPa). PaCO2 levels are equilibrated at approximately 2 mmHg above PwCO2 in each group (see text). The diagram also carries data (white symbols) replotted from McKenzie et al. (2002Go) describing blood acid–base status following acute sequential 30 min exposures to PwCO2 levels of 5, 10, 20, 40, 60 and 80 mmHg. The dashed line indicates the in vitro whole blood non-HCO3 buffer line for A. rostrata provided by Hyde et al. (1987Go). Values are means ± S.E.M., N=5–7 determinations.

 


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Fig. 2. The relationship between plasma concentrations of chloride and bicarbonate in eels exposed for at least 6 weeks to water CO2 partial pressures (PwCO2) of approx. 0.8 mmHg (ambient control), 15±1 mmHg, 30±1 mmHg or 45±1 mmHg (1 mmHg=approx. 0.01316 kPa). The black symbols indicate individual data points, the white symbols denote the mean values for each PwCO2. The regression line for the individual data points is described by the linear relationship [HCO3]=–0.817[Cl]+128 (r2=0.536, N=24), with concentrations in mmol l–1.

 


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Fig. 3. (A) The effects of increasing arterial CO2 partial pressures PaCO2 on arterial total O2 content (CaO2), expressed as the percentage change relative to normocapnia, in eels exposed either to chronic (black symbols) or acute (white symbols) hypercapnia. (B) The relationship between arterial blood pH (pHa) and CaO2 in eels exposed to either chronic (black symbols) or acute (white symbols) hypercapnia. Chronic hypercapnia implies at least 6 weeks exposure to water CO2 partial pressures (PwCO2) of approx. 2mmHg (ambient control), 15±1 mmHg, 30±1 mmHg or 45±1 mmHg; acute hypercapnia implies sequential 30 min exposures to a PwCO2 of 5, 10, 20, 40, 60 and 80 mmHg (1 mmHg=approx. 0.01316 kPa). Data for acute hypercapnia are replotted from McKenzie et al. (2002Go). Values are means ± S.E.M., N=5–7 determinations.

 


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Fig. 4. (A) The relationship between swimming speed and O2 uptake, and (B) between swimming speed and net cost of swimming (as O2 uptake; see text for details), in normocapnic control eels (red symbols and regression line) and in eels exposed for at least 6 weeks to a water CO2 partial pressure of 45±1 mmHg (blue symbols and regression line). In A, for control eels the relationship was described by the exponential equation y=2.85e1.20x (r2=0.699, N=23 observations on six animals), whereas for eels exposed to hypercapnia the equation was y=2.94e1.19x (r2=0.714, N=29 observations on seven animals). In B, for control eels the relationship was described by the power equation y=6.45x1.50 (r2=0.755, N=23 observations on six animals), whereas for eels exposed to hypercapnia the relationship was described by the equation y=6.51x1.70 (r2=0.739, N=29 observations on 7 animals).

 





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