The effects of hypercapnia (1% CO2), and the independent effects of changes in extracellular pH (pHe), PCO2 and [HCO3-] on intracellular pH (measured by the DMO method) and lactate metabolism (measured by utilization of 14C-labelled lactate), were examined in rainbow trout hepatocytes in vitro. Simulated uncompensated hypercapnia (high PCO2, low pHe, moderately increased [HCO3-] led to a substantial depression in the production of CO2 (44%) and glucose (51%) from lactate. In simulated compensated hypercapnia (high PCO2, normal pHe, high [HCO3-], metabolism was still significantly inhibited (18–33%). Subsequent multifactorial design experiments determined that variations in PCO2, pH and [HCO3-] independently affected metabolism; increased PCO2 and decreased pH inhibited metabolism, but increased [HCO3-] stimulated metabolism. These results are interpreted in terms of the effects of acid-base variables on enzymatic and transport pathways, and the possible causes of decreased hepatic glycogen stores during in vivo hypercapnia are discussed.

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