Abstract

Previous studies have demonstrated a constant fetal cerebral O2 consumpsion over a range of arterial O2 content (CaO2) from 5 to 1 mM. To determine the effect of such hypoxia on the “nonvital” tissues, we measured hindlimb O2 consumption (VO2) in 5 fetal sheep (8-16 days post-op). Four to six sample sets for hemoglobin concentration expressed as oxygen capacity and O2 saturation were drawn from the external iliac artery (IA) and vein during a control period and after equilibration at progressively decreasing levels of arterial O2 saturation (SaO2, %). Hypoxia was produced by maternal common internal iliac artery occlusion yielding fetal CaO2 from 4.93 to 0.95 mM. Blood flow (F, ml/min) to the pelvic limb was measured continuously with an ultrasonic blood flow transducer(Transonics Systems, Inc) placed around the IA. CaO2 (mM) and VO2 (μm/min) were calculated for each set. Hindlimb F had a tendency to increase while VO2 remained constant to a CaO2 ∼ 1.5 mM (SaO2 ∼ 25%), below which both F and VO2 fell sharply. We compared control with severe hypoxia (CaO2 <1.5 mM) by paired t-test. Results for the 5 animals expressed as mean ± sem are as follows: We conclude that 1) the fetus decreases F and VO2 to the pelvic limb in the face of severe hypoxia in order to preserve VO2 of vital organs such as brain, and 2) this decrease occurs at a well-defined level of fetal oxygenation.

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