Vasopressin Concentration in Amniotic Fluid as an Index of Fetal Hypoxia: Mechanism of Release in Sheep

Stark, Raymond I.; Daniel, Salha S.; Husain, Mazhar; Sanocka, Ulana; Zubrow, Alan B.; James, L. Stanley

doi:10.1203/00006450-198409000-00006

Cited by 10 publications

(9 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

Section: Discussionmentioning

confidence: 96%

“…Acute inhalational hypoxaemia was not associated with the passage of meconium in fetal sheep 6,7 , but rather with reduced peristalsis in the fetal gut 8 . In a small study of three animals, meconium was observed after 30 minutes partial umbilical cord occlusion resulting in hypoxia and acidosis 7 . Massive meconium release prior to fetal demise was noted after injection of sodium pentobarbital, probably related to terminal hypotension and loss of tone in the fetus 6 .…”

Section: Discussionmentioning

confidence: 96%

See 1 more Smart Citation

Meconium and fetal hypoxia: some experimental observations and clinical relevance

Westgate¹

2002

BJOG: An International Journal of Obstetrics and Gynaecology

View full text Add to dashboard Cite

In an experimental study, chemically sympathectomised near term fetal sheep and a control group were subjected to repeated episodes of acute hypoxia. Despite severe hypotension and metabolic acidosis, no animal in the control group had meconium-stained amniotic fluid, whereas every animal in the sympathectomised group had heavily meconium-stained amniotic fluid at the end of the experiments. These data and the available literature do not support a direct association between acute hypoxia and meconium-stained amniotic fluid but suggest that a reduction in sympathetic neural tone must be a component of meconium passage. Clinical and experimental data on the occurrence of meconium-stained amniotic fluid are reviewed.

show abstract

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 96%

Meconium and fetal hypoxia: some experimental observations and clinical relevance

Westgate¹

2002

BJOG: An International Journal of Obstetrics and Gynaecology

View full text Add to dashboard Cite

show abstract

“…A nega tive correlation to 1-min Apgar scores and Fi02 is shown. Therefore, hypoxia during birth is obviously one of the nonosmotic stimuli for AVP release [2, 3,14,15]. The degree of asphyxia is correlated with high AVP serum concentrations [6] and some in fants develop the syndrome of inappropriate AVP secretion [10], Additionally, increased intracranial pres sure stimulates AVP secretion [4].…”

Section: Discussionmentioning

confidence: 99%

The Role of Arginine-Vasopressin in the Regulation of Water Metabolism in Preterm Infants in the First Days of Life

Stegner¹,

Henkel²,

Commentz³

1987

Horm Res

View full text Add to dashboard Cite

We studied the role of arginine-vasopressin (AVP) in the regulation of fluid homeostasis in preterm infants. Group 1 was fed orally, groups 2 and 3 received fluids parenterally, and group 3 developed respiratory distress syndrome (RDS) and had to be ventilated. The infants of group 3 were not able to excrete the administered fluid, gained weight and consecutively developed hyponatremia. 1 -min Apgar scores as well as log FiO₂ correlated significantly with urinary AVP excretion on day 1. We conclude that nonosmotic stimuli are involved in the release of AVP and therefore disturb fluid homeostasis in severely ill infants with RDS.

show abstract

“…Each sample was replaced with an equivalent amount of normal saline solution. The volume of blood withdrawn over the 2-h period of these experiments has been shown not to affect vasopressin levels (10).…”

Section: Surgerymentioning

confidence: 99%

Plasma Vasopressin, Renin, and Catecholamines during Nitroprusside-Induced Maternal and Fetal Hypotension in Sheep

et al. 1988

Self Cite

View full text Add to dashboard Cite

ABSTRACT. The release of vasopressin, renin, and catecholamines by the fetus during either maternal or fetal hypotension was examined in chronically catheterized fetal lambs. Nitroprusside was infused intravenously for 1 h into seven pregnant ewes (maternal hypotension) or nine fetal lambs (fetal hypotension); the rates were adjusted to achieve a 15 to 30% decrease in mean blood pressure. During maternal hypotension, mean f S E vasopressin in maternal plasma increased from 1.2 f 0.2 pg.ml-' to 208 f 153 pg.ml-' and plasma renin activity increased from 1.5 f 0.3 ng.ml-'. h-' to 6.6 f 1.6 ng.ml-'. h-'. Fetal vasopressin and plasma renin activity also increased during the same interval from 1.1 f 0.3 to 16.9 +. 7.5 pg.ml-' and 3.7 f 1.1 to 10.5 f 2.85 ng.ml-'.h-', respectively; but no changes were observed in fetal blood pressure, heart rate, or acid base status. During fetal hypotension, mean vasopressin in fetal plasma increased from 4.3 f 3.4 pg. ml-' to 1054 f 772 pg.ml-', plasma renin activity increased from 5.7 f 2.2 ng . ml-' to 22.2 f 7.1 n g ml-' . h-', and total catecholamines from 174 f 58 pg . ml-' to 810 f 416 p g ml-'. There was no change in fetal heart rate, acid base status, osmolality, or sodium concentration. The fetus became and remained hypertensive for at least 1 h after the end of infusion. This prolonged hypertension was associated with elevated levels of vasopressin and plasma renin activity. Peak vasopressin levels were proportional to the total nitroprusside dose in both the ewe and fetus (maternal r = 0.796, fetus r = 0.870). These experiments indicate that as in the adult, vasopressin and the reninangiotensin system in the fetus are stimulated by euvolemic hypotension and may play an important role in the maintenance of fetal blood pressure during an hypotensive challenge. We speculate that the prolonged rebound hypertension represents immaturity of the fetus to fine tune the regulation, release, or metabolism of vasoactive mediators. More likely, the hypertension and elevated hormone levels represent homeostatic mechanisms to combat the nitroprusside-induced diminished cardiac output. Lastly, fetal release of vasopressin, renin-angiotensin, and norepinephrine during maternal hypotension suggests that they are sensitive indicators of early fetal compromise. 7The fetus may be compromised by episodes of maternal hypotension (postural changes, regional anesthesia, placenta previa, etc.) or fetal hypotension (cord occlusion, fetal blood loss secondary to abruptio placentae, etc.) (1). In adults of several species, hypotension is known to stimulate several vasoactive systems which act to restore blood pressure towards normal values (2-8).The ability of the fetus to similarly withstand hypotension may have a significant influence on subsequent short-term and longterm outcome. The present studies were undertaken to determine the fetal response to both maternal and fetal hypotension with respect to fetal release of vasopressin, renin, and catecholamines in the maintenance of fetal blood pressur...

show abstract

Vasopressin Concentration in Amniotic Fluid as an Index of Fetal Hypoxia: Mechanism of Release in Sheep

Cited by 10 publications

References 14 publications

Meconium and fetal hypoxia: some experimental observations and clinical relevance

Meconium and fetal hypoxia: some experimental observations and clinical relevance

The Role of Arginine-Vasopressin in the Regulation of Water Metabolism in Preterm Infants in the First Days of Life

Plasma Vasopressin, Renin, and Catecholamines during Nitroprusside-Induced Maternal and Fetal Hypotension in Sheep

Contact Info

Product

Resources

About