The Influence of Experimental Anaemia On Blood Acid-Base Regulation In Vivo and In Vitro in the Starry Flounder (Platichthys Stellatus) and the Rainbow Trout (Salmo Gairdneri)

Open Access
Publisher Website
Google Scholar
Abstract
Severe experimental anaemia caused a rise in Pcoco2 and an associated fall in pH (respiratory acidosis) in arterial and venous blood of both flounder and trout in vivo. In some trout, but not in flounder, there was also a rise in blood lactate, indicating metabolic acidosis. In vitro, blood buffer capacities declined with haematocrit, a factor which contributed to the extent of the acidoses in vivo. However, haematocrit did not influence the pK1 of the plasma HCO3−/H2CO3 system or the actual measurement of blood pH. The Donnan ratio for HCO3− varied linearly with pH over the range 7.0–7.6, indicating a passive distribution of HCO3− across the trout erythrocyte. The present data, together with other recent results, indicate that the teleost red blood cell does play a role in plasma HCO3− dehydration and CO2 excretion, and therefore opposes the theory of Haswell & Randall (1978) that the erythrocyte is functionally impermeable to HCO3−.

This publication has 22 references indexed in Scilit: