Increased urinary flow without development of polyhydramnios in response to prolonged hypoxia in the ovine fetus.
OBJECTIVE
In the ovine fetus subjected to 24 hours of hypoxia, urinary flow is normal within a few hours from the onset of hypoxia and there is a maintained inhibition of swallowing. We hypothesized that 4 days of fetal hypoxia would lead to polyhydramnios.


METHODS
Five late-gestation fetal sheep were subjected to hypoxia for 4 days and 7 other late-gestation fetal sheep served as time control animals. Fetal hypoxia was produced on postsurgical days 5 through 9 by continuous intratracheal nitrogen insufflation to the ewe. On days 3, 5, 7, and 9 after surgery, amniotic fluid volume, fetal urinary flow rate, and the compositions of maternal and fetal blood, amniotic fluid, and fetal urine were measured. A 3-factor analysis of variance was used for statistical analysis.


RESULTS
During the period of experimental hypoxia the mean (+/-SE) fetal PaO(2) was 16.0 +/- 0.6 mm Hg, versus 21.2 +/- 0.7 mm Hg in control sheep (P <.001). Fetal hypoxia was associated with increased urinary flow on days 7 and 9, averaging 1410 +/- 310 and 2101 +/- 345 mL/d, respectively, versus 585 +/- 92 and 699 +/- 78 mL/d, respectively, in control animals (P <.001). Amniotic fluid volume was unchanged with time and averaged 960 +/- 159 mL in hypoxic fetuses on postsurgical days 7 through 9 and 851 +/- 130 mL in control animals (P =.60). Fetal blood lactate increased in the hypoxic animals, averaging 3.4 +/- 2.1 mmol/L versus 1.6 +/- 0.3 mmol/L in control animals (P =.02). Fetal urinary excretions of sodium, potassium, chloride, and lactate increased significantly during hypoxia, by 170% to 400%.


CONCLUSIONS
Four days of nitrogen-induced hypoxia in the ovine fetus resulted in excess fetal urinary flow approximating 1000 mL/d greater than normal without the development of polyhydramnios. Because amniotic fluid volume did not change and hypoxia is a known inhibitor of fetal swallowing, we speculate that intramembranous absorption of amniotic water, electrolytes, and lactate increased.
Matsumoto
L C
LC
Division of Perinatal Medicine, Department of Reproductive Medicine, University of California at San Diego. La Jolla 92093-0802, USA.
Cheung
C Y
CY
Brace
R A
RA
D000653:Amniotic Fluid / Q000378:metabolism / Q000502:physiology*; D000818:Animals; D002245:Carbon Dioxide / Q000097:blood; D002712:Chlorides / Q000097:blood / Q000378:metabolism / Q000652:urine; D005260:Female; D005311:Fetal Hypoxia / Q000378:metabolism / Q000503:physiopathology* / Q000652:urine; D006863:Hydrogen-Ion Concentration; D019344:Lactic Acid / Q000097:blood / Q000652:urine; D010100:Oxygen / Q000097:blood; D006831:Polyhydramnios / Q000209:etiology* / Q000652:urine; D011188:Potassium / Q000097:blood / Q000378:metabolism / Q000652:urine; D011247:Pregnancy; D012756:Sheep / Q000196:embryology*; D012964:Sodium / Q000097:blood / Q000378:metabolism / Q000652:urine; D014563:Urodynamics
D002712:Chlorides; D002245:Carbon Dioxide; D019344:Lactic Acid; D012964:Sodium; D011188:Potassium; D010100:Oxygen