Splanchnic lactic acid metabolism in hyperventilation, metabolic alkalosis and shock

Abstract

Hyperlactatemia was induced in dogs by vigorous hyperventilation, shock or bicarbonate infusion, and blood was sampled from the aorta, hepatic vein and lower inferior vena cava. Hyperventilation with air caused elevated arterial lactate levels, an outpouring of lactate and glucose from the splanchnic bed and lactate uptake by hind-limb tissues. lactic acid extration by the splanchnic tissues began soon after cessation of hyperventilation. Hyperventilation was associated with declines in blood pressure, hepatic blood flow and hepatic vein oxygen tension, and increased hepatic vein lactate:pyruvate ratios. Pharmacologic or hemorrhagic shock also caused release of lactic acid from the splanchnic bed which was reversed during recovery. Bicarbonate infusion caused hyperlactatemia not associated with splanchnic output of lactic acid. Experiments with isolated perfused rat liver demonstrated that alkalotic perfusion or ischemia could stimulate hepatic release of lactate. Pyruvate uptake and increased glucose output occurred only in hypoxia. These experiments indicate that the changes in splanchnic lactic acid and glucose metabolism in hyperventilation and shock are due to hepatic ischemia and suggest that the liver may play a major role in the pathogenesis of lactic acidosis.