Gill ventilation, blood gas and acid‐base values, Ṁ O 2 , Ṁ CO 2 and the gas exchange ratio have been measured before, during, and after exposure to hypoxia in the channel catfish, Ictalurus punctatus. I. punctatus maintains Ṁ O 2 at control levels to a P IO 2 as low as 60 mm Hg, through a profound branchial hyperventilation. Concomitantly, however, a lactic acidosis usually develops, indicating a significant anaerobic glycolysis. Both a metabolic acidosis and respiratory alkalosis occur in Ictalurus during hypoxic exposure, with the former usually predominating. Ṁ CO 2 doubles and the gas exchange ratio (R E ) increases from 0.8 at control levels to 2.0 at hypoxic levels, indicating that, in addition to anaerobic glycolysis, nonglycolytic pathways producing CO 2 also operate during hypoxic exposure. Analysis reveals that at least half of the increased Ṁ CO 2 during hypoxic exposure is due strictly to lactate acidfication of the tissue HCO 3 − pool, rather than from metabolic production of molecular CO 2 . Thus, the actual respiratory quotient (R Q ) only rises to 1.5 during hypoxic exposure. Within one hour of a return to air saturated water, a large lactate “flush” and severe plasma acidosis occur, and control levels for these and other values are not reachieved for 2–6 hours after hypoxic exposure. Complete analysis of O 2 and CO 2 exchange in the catfish exposed to short‐term hypoxia thus must consider both the time course of acid‐base disturbance and the evolution of CO 2 from the acidified tissue bicarbonate pool.
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Burggren et al. (1980) studied this question.
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