The effects of changes in environmental temperature and oxygen tension on gill ventilation, arterial PO2, PCO2 pH and [HCO3] were evaluated in carp (Cyprinus carpio L.). Gill ventilation was measured continuously in specimens acclimated to 10 or 20°C, combining the method of electromagnetic flow determination with the application of a rubber mask technique. After establishing control values in airequilibrated water the environmental water PO2 (PwO2) was reduced from about 150 mmHg (20 kPa) during control conditions to 110 or 75 mm Hg (14.7 or 10 kPa), respectively. Measurements of blood gases and acid-base parameters were performed repeatedly before, and 1 and 4 h after, initiation of hypoxia. Regardless of temperature, these moderately hypoxic conditions caused considerable and lasting increases in gill ventilation of about 70% (PWO2=110 mm Hg/l4.7kPa) or 180% (PwO2=75 mm Hg/10kPa), relative to the respective normoxic control values of about 50 ml kg−1min−1 at 10°C and 230 ml kg −1min−1 at 20°C. These increases in ventilation reduced PCO2 substantially, resulting in a rise in pHa by about 0.1 units at PwO2 of 110 mmHg (14.7 kPa) and by about 0.2 units at PwCO2 of 75 mmHg (lOkPa). Arterial PO2 was low under normoxic conditions at both temperatures (≈15 mmHg, ≈2kPa). During hypoxia, PaO2 was marginally reduced, whereas the arterial O2 content and saturation remained at normoxic levels, mainly because of the increase in the blood O2-affinity induced by respiratory alkalosis. Thislack of any clear relationship between arterial O2 content and ventilatory response to moderate hypoxia contrasts with previously reported data for trout, and supports the hypothesis that a change in PO2 is an adequate stimulus for the adjustment of ventilation in carp.

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