Intravascular infusions of plasma into fetal sheep cause arterial and venous hypertension

George Giraud, J. Job Faber, Sonnet Jonker, Lowell Davis, Debra Anderson

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Fetal volume control is driven by an equilibrium between fetal and maternal hydrostatic and oncotic pressures in the placenta. Renal contributions to blood volume regulation are minor because the fetal kidneys cannot excrete fluid from the fetal compartment. We hypothesized that an increase in fetal plasma protein would lead to art increase in plasma oncotic pressure, resulting in an increase in fetal arterial and venous pressures and decreased angiotensin levels. Plasma or lactated Ringer solution was infused into each of five twin fetuses. After 7 days, fetal protein concentration was 71.2 ± 4.2 g/l in the plasma-infused fetuses compared with 35.7 ± 6.3 g/l in the lactated Ringer-solution-infused fetuses. Arterial pressure was 68.0 ± 3.6 compared with 43.4 ± 1.9 mmHg in the lactated Ringer solution-infused fetuses (P <0.0003), whereas venous pressure was 4.8 ± 0.3 mmHg in the plasma-infused fetuses compared with 3.3 ± 0.4 mmHg in the lactated Ringer solution-infused fetuses (P <0.036). Six fetuses were studied on days 0, 7, and 14 of plasma protein infusion. Fetal protein concentration increased from 31.1 ± 1.5 to 84.8 ± 3.8 g/l after 14 days (P <0.01), and arterial pressure increased from 43.1 ± 1.8 to 69.1 ± 4.1 mmHg (P <0.01). Venous pressure increased from 3.0 ± 0.4 to 6.2 ± 1.3 mmHg (P <0.05). Fetal heart rate did not change. Angiotensin II concentration decreased, from 24.6 ± 5.6 to 2.9 ± 1.3 pg/l, after 14 days (P <0.01). Fetal plasma infusions resulted in fetal arterial and venous hypertensions that could not be corrected by reductions in angiotensin II levels.

Original languageEnglish (US)
Pages (from-to)884-889
Number of pages6
JournalJournal of Applied Physiology
Volume99
Issue number3
DOIs
StatePublished - Sep 2005

Fingerprint

Sheep
Fetus
Hypertension
Fetal Proteins
Venous Pressure
Arterial Pressure
Angiotensin II
Blood Proteins
Kidney
Fetal Heart Rate
Hydrostatic Pressure
Angiotensins
Art
Blood Volume
Placenta
Mothers
Pressure
Ringer's lactate
Ringer's solution

Keywords

  • Angiotensin
  • Blood pressure
  • Renin

ASJC Scopus subject areas

  • Physiology
  • Endocrinology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Intravascular infusions of plasma into fetal sheep cause arterial and venous hypertension. / Giraud, George; Faber, J. Job; Jonker, Sonnet; Davis, Lowell; Anderson, Debra.

In: Journal of Applied Physiology, Vol. 99, No. 3, 09.2005, p. 884-889.

Research output: Contribution to journalArticle

@article{6eb437880b6244919a6f50466f115acb,
title = "Intravascular infusions of plasma into fetal sheep cause arterial and venous hypertension",
abstract = "Fetal volume control is driven by an equilibrium between fetal and maternal hydrostatic and oncotic pressures in the placenta. Renal contributions to blood volume regulation are minor because the fetal kidneys cannot excrete fluid from the fetal compartment. We hypothesized that an increase in fetal plasma protein would lead to art increase in plasma oncotic pressure, resulting in an increase in fetal arterial and venous pressures and decreased angiotensin levels. Plasma or lactated Ringer solution was infused into each of five twin fetuses. After 7 days, fetal protein concentration was 71.2 ± 4.2 g/l in the plasma-infused fetuses compared with 35.7 ± 6.3 g/l in the lactated Ringer-solution-infused fetuses. Arterial pressure was 68.0 ± 3.6 compared with 43.4 ± 1.9 mmHg in the lactated Ringer solution-infused fetuses (P <0.0003), whereas venous pressure was 4.8 ± 0.3 mmHg in the plasma-infused fetuses compared with 3.3 ± 0.4 mmHg in the lactated Ringer solution-infused fetuses (P <0.036). Six fetuses were studied on days 0, 7, and 14 of plasma protein infusion. Fetal protein concentration increased from 31.1 ± 1.5 to 84.8 ± 3.8 g/l after 14 days (P <0.01), and arterial pressure increased from 43.1 ± 1.8 to 69.1 ± 4.1 mmHg (P <0.01). Venous pressure increased from 3.0 ± 0.4 to 6.2 ± 1.3 mmHg (P <0.05). Fetal heart rate did not change. Angiotensin II concentration decreased, from 24.6 ± 5.6 to 2.9 ± 1.3 pg/l, after 14 days (P <0.01). Fetal plasma infusions resulted in fetal arterial and venous hypertensions that could not be corrected by reductions in angiotensin II levels.",
keywords = "Angiotensin, Blood pressure, Renin",
author = "George Giraud and Faber, {J. Job} and Sonnet Jonker and Lowell Davis and Debra Anderson",
year = "2005",
month = "9",
doi = "10.1152/japplphysiol.01429.2004",
language = "English (US)",
volume = "99",
pages = "884--889",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "3",

}

TY - JOUR

T1 - Intravascular infusions of plasma into fetal sheep cause arterial and venous hypertension

AU - Giraud, George

AU - Faber, J. Job

AU - Jonker, Sonnet

AU - Davis, Lowell

AU - Anderson, Debra

PY - 2005/9

Y1 - 2005/9

N2 - Fetal volume control is driven by an equilibrium between fetal and maternal hydrostatic and oncotic pressures in the placenta. Renal contributions to blood volume regulation are minor because the fetal kidneys cannot excrete fluid from the fetal compartment. We hypothesized that an increase in fetal plasma protein would lead to art increase in plasma oncotic pressure, resulting in an increase in fetal arterial and venous pressures and decreased angiotensin levels. Plasma or lactated Ringer solution was infused into each of five twin fetuses. After 7 days, fetal protein concentration was 71.2 ± 4.2 g/l in the plasma-infused fetuses compared with 35.7 ± 6.3 g/l in the lactated Ringer-solution-infused fetuses. Arterial pressure was 68.0 ± 3.6 compared with 43.4 ± 1.9 mmHg in the lactated Ringer solution-infused fetuses (P <0.0003), whereas venous pressure was 4.8 ± 0.3 mmHg in the plasma-infused fetuses compared with 3.3 ± 0.4 mmHg in the lactated Ringer solution-infused fetuses (P <0.036). Six fetuses were studied on days 0, 7, and 14 of plasma protein infusion. Fetal protein concentration increased from 31.1 ± 1.5 to 84.8 ± 3.8 g/l after 14 days (P <0.01), and arterial pressure increased from 43.1 ± 1.8 to 69.1 ± 4.1 mmHg (P <0.01). Venous pressure increased from 3.0 ± 0.4 to 6.2 ± 1.3 mmHg (P <0.05). Fetal heart rate did not change. Angiotensin II concentration decreased, from 24.6 ± 5.6 to 2.9 ± 1.3 pg/l, after 14 days (P <0.01). Fetal plasma infusions resulted in fetal arterial and venous hypertensions that could not be corrected by reductions in angiotensin II levels.

AB - Fetal volume control is driven by an equilibrium between fetal and maternal hydrostatic and oncotic pressures in the placenta. Renal contributions to blood volume regulation are minor because the fetal kidneys cannot excrete fluid from the fetal compartment. We hypothesized that an increase in fetal plasma protein would lead to art increase in plasma oncotic pressure, resulting in an increase in fetal arterial and venous pressures and decreased angiotensin levels. Plasma or lactated Ringer solution was infused into each of five twin fetuses. After 7 days, fetal protein concentration was 71.2 ± 4.2 g/l in the plasma-infused fetuses compared with 35.7 ± 6.3 g/l in the lactated Ringer-solution-infused fetuses. Arterial pressure was 68.0 ± 3.6 compared with 43.4 ± 1.9 mmHg in the lactated Ringer solution-infused fetuses (P <0.0003), whereas venous pressure was 4.8 ± 0.3 mmHg in the plasma-infused fetuses compared with 3.3 ± 0.4 mmHg in the lactated Ringer solution-infused fetuses (P <0.036). Six fetuses were studied on days 0, 7, and 14 of plasma protein infusion. Fetal protein concentration increased from 31.1 ± 1.5 to 84.8 ± 3.8 g/l after 14 days (P <0.01), and arterial pressure increased from 43.1 ± 1.8 to 69.1 ± 4.1 mmHg (P <0.01). Venous pressure increased from 3.0 ± 0.4 to 6.2 ± 1.3 mmHg (P <0.05). Fetal heart rate did not change. Angiotensin II concentration decreased, from 24.6 ± 5.6 to 2.9 ± 1.3 pg/l, after 14 days (P <0.01). Fetal plasma infusions resulted in fetal arterial and venous hypertensions that could not be corrected by reductions in angiotensin II levels.

KW - Angiotensin

KW - Blood pressure

KW - Renin

UR - http://www.scopus.com/inward/record.url?scp=24044432256&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=24044432256&partnerID=8YFLogxK

U2 - 10.1152/japplphysiol.01429.2004

DO - 10.1152/japplphysiol.01429.2004

M3 - Article

C2 - 15879162

AN - SCOPUS:24044432256

VL - 99

SP - 884

EP - 889

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 3

ER -