HYPOXIA EFFECTS ON AMNIOTIC FLUID VOLUME
缺氧对羊水量的影响
基本信息
- 批准号:2692264
- 负责人:
- 金额:$ 27.5万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1998
- 资助国家:美国
- 起止时间:1998-07-01 至 2003-04-30
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Normal amounts of amniotic fluid must be present in order for the fetus
to grow and develop normally. Oligohydramnios (too little amniotic
fluid) occurs in approximately 5 percent of human pregnancies and is
responsible for many emergency cesarean sections, in utero fetal deaths
due to cord compression, and neonatal deaths due to respiratory
distress. Although it is widely assumed that fetal hypoxia causes
oligohydramnios, the effects of hypoxia on amniotic fluid volume have
not been studied experimentally. Indirect evidence suggests that fetal
hypoxia may actually cause polyhydramnios (too much amniotic fluid)
rather than oligohydramnios. The proposed studies will determine the
effects of hypoxia on amniotic fluid volume in fetal sheep and explore
the mechanisms of these effects. The overall hypothesis is that fetal
hypoxia produces polyhydramnios and that fetal hypoxia in combination
with placental insufficiency causes oligohydramnios. In Specific Aim
number 1, fetal hypoxia will be produced by progressive fetal anemia
(anemic hypoxia). The hypothesis is that there will be a threshold at
which a large increase in amniotic fluid volume occurs and this is
dependent upon elevated fetal plasma lactate and arginine vasopressin
levels. In Specific Aim number 2, the fetus will be made hypoxic by
reducing the inspired oxygen content of the mother (hypoxic hypoxia).
The hypothesis is that polyhydramnios will develop and the associated
mechanisms are the same as occur during anemic hypoxia. In Specific Aim
number 3, the fetus will be made hypoxic by repeated microsphere
embolizations of the umbilical circulation. The hypothesis is that this
combination of fetal hypoxia and placental insufficiency will produce
oligohydramnios. For each of these Specific Aims, the associated
mechanisms will be studied by monitoring fetal urine production, fetal
swallowing, lung liquid secretion, and the volume of amniotic fluid
absorbed via the intramembranous pathway. Specific changes in each of
these four flows are hypothesized for each method of creating fetal
hypoxia. We expect the changes in amniotic fluid volume to be
accurately predicted from the four measured flows. Overall, the proposed
studies are important because they will dramatically improve our
understanding of amniotic fluid volume regulation in the fetus under
normoxic and hypoxic conditions. This is relevant clinically because an
increased understanding of the mechanisms which regulate amniotic fluid
volume should lead to better therapies for maintaining normal amniotic
fluid volumes during human pregnancy and this would help reduce fetal
and neonatal morbidity and mortality.
为了胎儿的发育,必须有正常数量的羊水
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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ROBERT A BRACE其他文献
ROBERT A BRACE的其他文献
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{{ truncateString('ROBERT A BRACE', 18)}}的其他基金
REGULATION OF ERYTHROPOIETIN GENE EXPRESSION IN FETUS
胎儿促红细胞生成素基因表达的调控
- 批准号:
2889212 - 财政年份:1997
- 资助金额:
$ 27.5万 - 项目类别:
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