SUMMARY

To study both temporal and quantitative effects of hypercapnia on the extent of pH compensation in the arterial blood, specimens of carp (Cyprinus carpio) were exposed to a Pcc,2 of about 7-5mmHg (1 mmHg = 133-3Pa) ( 1 % CO2) in the environmental water for several weeks, and a second group of animals was subjected to an environmental Pco2 of about 37 mmHg (5 % CO2) for up to 96 h. A third series of experiments was designed to test the possibility that infusion of bicarbonate would increase the extent of plasma pH compensation. Dorsal aortic plasma pH, Pcoj and [HCO3~], as well as net transfer of HCO3~-equivalent ions, NH4 +, Cl ~ and Na+, between fish and ambient water, were monitored throughout the experiments. Exposure to environmental PCOz of 7-5 mmHg resulted in the expected respiratory acidosis with the associated drop in plasma pH, and subsequent compensatory plasma [HCO3~] increase. The compensatory increase of plasma bicarbonate during long-term hypercapnia continued during 19 days of exposure with plasma bicarbon-ate finally elevated from 13-0mmoll~ ' during control conditions to 25-9mmol I"1 in hypercapnia, an increase equivalent to 80 % plasma pH compensation