A Comparison of CO2 Excretion in A Spontaneously Ventilating Blood-Perfused Trout Preparation and Saline-Perfused Gill Preparations: Contribution of the Branchial Epithelium and Red Blood Cell

Abstract

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. CO2 excretion blood-perfused preparations was positively correlated with haematocrit (Het), and was abolished completely during plasma-perfusion. Elevating HCO3− concentration of input blood from 10 to 25 mm significantly increased , fourfold in blood-perfused preparations as a result of increased entry of HCO3− 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′-iro-thiocyanatostilbene-2,2′ disulfonic acid (SITS; 10−4 M) to input blood significantly reduced and oxygen uptake in blood-perfused fish due to inhibition of erythrocytic HCO3Ȓ/Cl −exchange. Unlike blood-perfused preparations, no saline-perfused preparation (isolated holobranchs or totally perfused rainbow trout or coho salmon) displayed measureable CO2 excretion at physiological and pH. Increased input in both blood-perfused and saline-perfused preparations significantly increased 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 CO2 excretion and that movement of HCO3− from plasma to gill epithelium cells in no way contributes to overall CO2 elimination.