AJP - Regulatory, Integrative and Comparative Physiology, Vol 266, Issue 6 1759-R1764, Copyright © 1994 by American Physiological Society
Renal function during chronic anemia in the ovine fetus
L. E. Davis, A. R. Hohimer and L. L. Woods
Department of Obstetrics, Oregon Health Sciences University, Portland 97201-3098.
Our purpose was to determine how prolonged anemia alters fetal renal
function and acid-base balance. In seven ovine fetuses made progressively
anemic over 1 wk by serial isovolemic hemorrhage, hematocrit was reduced
from 33.3 +/- 4.5 to 14.0 +/- 1.0%. Femoral arterial oxygen content was
less and renal plasma flow was greater in anemic fetuses (1.5 +/- 0.1 ml/dl
and 339 +/- 58 ml.min-1.100 g kidney-1) than in 6 control fetuses (7.0 +/-
1.3 ml/dl and 160 +/- 34 ml.min-1.100 g kidney-1). Urine flow and sodium
excretion were also greater in anemic fetuses (1.2 +/- 0.6 ml/min and 79
+/- 49.5 mumol/min) than in controls (0.5 +/- 0.2 ml/min and 16 +/- 9.8
mumol/min). This higher sodium excretion was apparently due to a lower
fractional sodium reabsorption in anemic fetuses compared with controls
(84.1 +/- 5.8 vs. 96.5 +/- 1.7%), rather than to differences in either
glomerular filtration rate or amount of filtered sodium. In addition, the
higher sodium excretion in anemic fetuses was associated with greater
urinary lactate and inorganic phosphate excretions and larger amniotic
fluid volumes than in controls. From these data we conclude that when fetal
renal oxygen delivery is limited by a prolonged reduction in hematocrit,
excretions of sodium and water, as well as other osmotically active
solutes, increase, and this results in an increase in amniotic fluid
volume.
