Abstract

Acid-base balance changes as well as rises in erythropoietin (Ep) levels were studied in rabbits during the first 12 h of either anemic or hypobaric hypoxia and following CoC<sub>2</sub> treatment. Bleeding and CoCl<sub>2</sub> administration lead to an early and transient decrease in blood pH associated with a rise in blood lactate. Hypobaric exposure causes alkalosis and lactate increase, both persisting at 12 h. Both hypobarism and CoCl<sub>2</sub> treatment lead to decrease in pCO<sub>2</sub>, which is far greater than after bleeding. Only hypobaric exposure produces a rise in erythrocyte 2,3-DPG; in addition, it leads to far higher plasma Ep levels than bleeding or CoCl<sub>2</sub> treatment. It is unlikely that pCO<sub>2</sub> lowering plays a determinant role in Ep production, while a possible enhancing effect of blood pH other than Bohr effect remains quite hypothetic. Ep production seems to be actually correlated with blood lactate increases, in agreement with a regulatory role of this metabolite on Ep production suggested by other authors.

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