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Acid-base balance in arterial plasma of white Pekin duck (Anas platyrhynchos) during forced submergence and recovery Shimizu, Manabu

Abstract

Acid-base balance in plasma was studied in forcibly submerged Pekin ducks (Anas platyrhynchos). All important variables determining acid-base balance (arterial CO₂ tension (PαCO₂) strong ion difference ([SID]) and total protein content which approximates total weak acid concentration in plasma) were measured. During forced submergence PαCO₂ increased and pHa steadily decreased with time. There was also an increase in [lactate⁻], which was accompanied by an increase of equal magnitude in [Na⁺]. There were no significant changes in the concentrations of other strong ions (K⁺, Ca²⁺, Mg²⁺ and Cl⁻). Strong ion difference did not change during the first two minutes of submergence, but there was about a 4 mequiv/L increase by the end of the four-minute dive. Theoretically an increase in [SID] should cause plasma to be alkaline, but since plasma became progressively acidic, this condition can only be due to the increase in PαCO₂. During recovery from dives, the plasma remained as acidic one minute after emersion as at the end of the dives. On the other hand, arterial pH slowly increased towards the pre-dive level during recovery. Arterial CO₂ tension decreased much more rapidly and was already at or below the pre-dive level one minute after emersion. Therefore, PαCO₂ could no longer affect plasma pH. There was, however, a great increase in [lactate-] in the first minute of recovery. Although [Na⁺] and [K⁺] were elevated, from pre-dive values after the four minute dive, the increase in [lactate⁻] resulted in a marked reduction in [SID]. Since there was no change in the total plasma protein content, the acidic condition observed in recovery could only be due to decreased [SID]. Breathing 0₂ before diving prevented circulatory adjustments and pH returned to pre-dive levels one minute after emersion, confirming that the acidic condition observed in recovery is a consequence of the lactate produced in the hypoperfused tissues during submergence.

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