Effects of hypoxia on choline exchange among organs

Cerebral blood flow (CBF) and the arteriovenous (A-V) difference for choline (Ch) across brain, lung, splanchnic territory, liver, kidney, and lower limb were studied in anesthetized, mechanically ventilated rats subjected to 10-20-min periods of hypoxia induced by lowering the inspired O2 concentration to 13%. A large, time-dependent increase in arterial blood Ch concentration occurred during hypoxia. This phenomenon coincided with a net rate of uptake of Ch by the brain during hypoxia (0.81 +/- 0.24 nmol/min, n = 10; p less than 0.05), which contrasted with a net rate of loss of Ch by this organ during the control period that preceded hypoxia (-0.20 +/- 0.08 nmol/min, n = 10; p less than 0.05). During hypoxia, lungs and splanchnic territory showed negative A-V differences for Ch levels (net Ch loss), whereas brain, liver, kidney, and lower limb showed positive A-V differences for Ch levels (net Ch uptake). Ch output from lungs was already detected at 5 min within the period of hypoxia and reversed rapidly after restoration of normal oxygenation. On the other hand, Ch output from the splanchnic territory became evident only 10 min after commencement of hypoxia and outlasted this experimental condition. It is concluded that extracerebral production of Ch during hypocapnic hypoxia raises the arterial concentration of this molecule and, by reversing the gradient across cerebral capillaries, prevents the cerebral loss of Ch in this condition.