Splanchnic vasomotor and metabolic adjustments to hypoxia and exercise in humans

Abstract

To determine whether hypoxia increases splanchnic vasoconstriction and impedes splanchnic metabolism during exercise, 11 subjects were exercised for 72 min at O2 uptake (.ovrhdot.VO2) of 1.8 l/min; 11% O2 was breathed during 30-50 min. Splanchnic blood flow (SBF), arterial and hepatic venous concentrations of indocyanine green (ICG), O2, CO2, metabolites and catecholamines were determined in 7 subjects; complete sets of all measurements were obtained from 4. Arterial O2 content and tension fell from normal values to 12.3 ml/100 ml and to 32.2 Torr, respectively, during hypoxia; heart rate [HR] rose to 159 from 117 beats/min, arterial blood pressure was unchanged, and plasma norepinephrine (NE) and epinephrine (E) concentrations rose from 0.79 (NE) and 0.2 (E) ng/ml (normoxia) to 2.7 and 0.72, respectively, during hypoxia. SBF rose insignificantly from 1.14 (normoxia) to 1.35 l/min during hypoxia and fell significantly to 1.01 l/min after return to normoxia. Splanchnic .ovrhdot.VO2 was maintained at normal levels by increased extraction as hepatic venous O2 fell to 1.7 ml/100 ml and hepatic venous O2 tension to 7.5 Torr. Hepatic glucose release rose from 642 (normoxia) to 1164 mg/min (hypoxia); lactate uptake increased from 0.26 to 2.1 mM/min; NE uptake rose from 417 to 1,508 ng/min, but hypoxia reduced ICG extraction by 28%. Hypoxia did not cause splanchnic vasoconstriction normally accompanying increases in HR and NE concentration or reductions in maximum .ovrhdot.VO2. SBF was maintained at a level sufficient to maintain all metabolic functions except ICG extraction.