Oxygen consumption in the fetal lamb during sustained hypoxemia with progressive acidemia.
To investigate the fetal ability to compensate for a sustained reduction in O2 delivery (DO2; umbilical blood flow X umbilical venous O2 content), studies were carried out on eight chronically instrumented fetal lambs made hypoxemic for 7.8 +/- 0.8 (+/- SE) h by lowering maternal inspired O2 concentration to 9-10%. After 1.7 h of hypoxemia, fetal arterial PO2 had fallen from 18.4 +/- 1.2 to 10.4 +/- 0.5 mmHg. Umbilical venous O2 content fell initially by 41.1 +/- 1.8%, but the fall in DO2 was only 23.7 +/- 5.6%, caused by a 29.3 +/- 7.9% rise in umbilical blood flow. Fetal O2 consumption (VO2) was increased significantly by 29.5 +/- 15.2%. However, fetal vascular pH (7.332-7.281) and base excess (0.5 to -4.3 meq/l) were decreased while blood lactate levels were increased (1.55-7.22 mM). With continued hypoxemia, the metabolic acidemia worsened and led to progressive declines in umbilical venous O2 content and DO2. However, VO2 was maintained at the control level until delivery had fallen by 72.5% and arterial pH was 6.843, at which time VO2 decreased by 37.5 +/- 10.7%. It is concluded that the ability of the fetus to compensate for sustained hypoxemia is limited by the progressive metabolic acidemia.
Rurak
D W
DW
Department of Obstetrics and Gynaecology, University of Western Ontario, London, Canada.
Richardson
B S
BS
Patrick
J E
JE
Carmichael
L
L
Homan
J
J
D000136:Acid-Base Equilibrium; D000143:Acids / Q000097:blood*; D000818:Animals; D001682:Biological Availability; D001794:Blood Pressure; D005312:Fetal Blood; D005333:Fetus / Q000378:metabolism*; D005740:Gases / Q000097:blood; D006339:Heart Rate; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000378:metabolism*; D010100:Oxygen / Q000493:pharmacokinetics; D010101:Oxygen Consumption; D012039:Regional Blood Flow; D012756:Sheep
D000143:Acids; D005740:Gases; D010100:Oxygen