| pubmed-article:6465330 | pubmed:abstractText | To determine whether hypoxia increases splanchnic vasoconstriction and impedes splanchnic metabolism during exercise, 11 subjects were exercised for 72 min at O2 uptake (VO2) of 1.8 1/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 seven subjects; complete sets of all measurements were obtained from four. Arterial O2 content and tension fell from normal values to 12.3 ml/100 and to 32.2 Torr, respectively, during hypoxia; heart rate 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 1/min after return to normoxia. Splanchnic 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 1,164 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%. Thus hypoxia did not cause splanchnic vasoconstriction normally accompanying increases in HR and NE concentration or reductions in maximum VO2. SBF was maintained at a level sufficient to maintain all metabolic functions except ICG extraction. | lld:pubmed |
