Renal function during chronic anemia in the ovine fetus

Lowell Davis, Alan (Roger) Hohimer, L. L. Woods

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

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 μmol/min) than in controls (0.5 ± 0.2 ml/min and 16 ± 9.8 μmol/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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume266
Issue number6 35-6
StatePublished - 1994

Fingerprint

Anemia
Sheep
Fetus
Sodium
Kidney
Amniotic Fluid
Hematocrit
Oxygen
Renal Plasma Flow
Acid-Base Equilibrium
Thigh
Glomerular Filtration Rate
Lactic Acid
Phosphates
Urine
Hemorrhage
Water

Keywords

  • amniotic fluid volume
  • glomerular filtration rate
  • kidney
  • oxygen delivery
  • renal blood flow
  • sheep

ASJC Scopus subject areas

  • Physiology

Cite this

Renal function during chronic anemia in the ovine fetus. / Davis, Lowell; Hohimer, Alan (Roger); Woods, L. L.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 266, No. 6 35-6, 1994.

Research output: Contribution to journalArticle

@article{1c1dbebc0f5b4983b5275b5b27d2ed54,
title = "Renal function during chronic anemia in the ovine fetus",
abstract = "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 μmol/min) than in controls (0.5 ± 0.2 ml/min and 16 ± 9.8 μmol/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.",
keywords = "amniotic fluid volume, glomerular filtration rate, kidney, oxygen delivery, renal blood flow, sheep",
author = "Lowell Davis and Hohimer, {Alan (Roger)} and Woods, {L. L.}",
year = "1994",
language = "English (US)",
volume = "266",
journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "6 35-6",

}

TY - JOUR

T1 - Renal function during chronic anemia in the ovine fetus

AU - Davis, Lowell

AU - Hohimer, Alan (Roger)

AU - Woods, L. L.

PY - 1994

Y1 - 1994

N2 - 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 μmol/min) than in controls (0.5 ± 0.2 ml/min and 16 ± 9.8 μmol/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.

AB - 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 μmol/min) than in controls (0.5 ± 0.2 ml/min and 16 ± 9.8 μmol/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.

KW - amniotic fluid volume

KW - glomerular filtration rate

KW - kidney

KW - oxygen delivery

KW - renal blood flow

KW - sheep

UR - http://www.scopus.com/inward/record.url?scp=0028342679&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028342679&partnerID=8YFLogxK

M3 - Article

VL - 266

JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

SN - 1931-857X

IS - 6 35-6

ER -