A spontaneously ventilating blood-perfused trout preparation and saline perfused gill preparations were utilized to investigate the role of the erythrocyte and branchial epithelium in CO2 excretion and acid-base regulation.
CO, excretion (MCOCO2) in blood-perfused preparations was positively correlated with haematocrit (Hct), and was abolished completely during plasma-perfusion.
Elevating HCO3- concentration of input blood from 10 to 25 mM significantly increased MCOCO2. fourfold in blood-perfused preparations as a result of increased entry of HCO into the red blood cell and not into the gill epithelium. Increased HCO3- concentration was without effect in totally saline-perfused coho salmon (Onchorynchus kisutch).
The addition of 4-acetamido-4′-wo-thiocyanatostilbene-2, 2 disulfonic acid (SITS; 10−4 M) to input blood significantly reduced MCO, and oxygen uptake (Mg,OO2) in blood-perfused fish due to inhibition of erythrocytic HCO3-exchange.
Unlike blood-perfused preparations, no saline-perfused preparation (isolated holobranchs or totally perfused rainbow trout or coho salmon) displayed measureable CO, excretion at physiological Pco and pH.
Increased input PCOt in both blood-perfused and saline-perfused preparations significantly increased MCOt due to enhanced branchial diffusion of molecular CO2.
It is concluded that the entry of HCO3- into the erythrocyte is the rate-limiting step in CO, excretion and that movement of HCO3- from plasma to gill epithelium cells in no way contributes to overall CO3 elimination.
Note:
Department of Physiology and Anatomy, Massey University Palmerston North, New Zealand.
Pacific Gamefish Foundation, P.O. Box 25115, Honolulu, Hawaii, U.S.A. 96825
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