MATERNAL DEHYDRATION--FETAL & AMNIOTIC FLUID HOMEOSTASIS

母体脱水--胎儿

基本信息

项目摘要

Pregnant women may be exposed to exercise, thermal, or gastrointestinal (hyperemesis) water loss, all of which commonly induce a >10 mOsm increase in plasma osmolality (osm). Although fetal plasma is dependent on maternal osm the impact of maternal dehydration and subsequent rehydration on the fetus has not been explored. Increases in maternal plasma osm well within the physiologic range result in significant fetal endocrine responses (stimulation of arginine vasopressin and renin secretion and perhaps a suppression of atrial natriuretic factor) and subsequent alterations in fetal water dynamics and blood volume. Despite maternal rehydration, fetal endocrine and fluid responses persist beyond a return to basal maternal and fetal plasma osm. As a result, episodic maternal dehydration may contribute to the development of oligohydramnios, premature labor, and/or fetal growth retardation. This project will utilize the chronically catheterized ovine model to investigate the ontogeny of fetal and amniotic fluid water and electrolyte responses to maternal dehydration and subsequent rehydration. A compartmental model will be utilized to quantify alterations in fetal water acquisition (fetal swallowing and transplacental flow) and excretion (urine and lung fluid). Specifically, we have developed and confirmed a method for the measurement of fetal swallowing activity and volume. Fetal urine and lung fluid production will be measured directly, and transplacental flow calculated. The resultant effects on fetal blood volume and the impact on amniotic and allantoic water compartments will be evaluated. The response of selected fetal endocrine systems central to water homeostasis will be examined and the mechanisms of endocrine regulation of fetal fluid and electrolytes and swallowing responses will be studied using selective agonists and antagonists. As maternal and fetal responses to rehydration differ depending upon the mode of hydration, this project also will examine the fetal endocrine and fluid responses to several means of maternal rehydration. Studies of dehydration and rehydration of the ovine model represent a promising approach to understanding maternal-fetal water dynamics, while addressing a potentially critical problem in perinatal medicine.
孕妇可能会接触到运动、热疗或 胃肠道(呕吐)失水,所有这些通常 诱导血浆渗透压(OSM)升高10 mOsm。虽然 胎儿血浆对母体OSM的影响 胎儿的脱水和随后的复水还没有得到 探索过了。母体血浆OSM的增加在 生理范围导致显著的胎儿内分泌反应 (刺激精氨酸加压素和肾素的分泌和 可能是心钠素的抑制)和随后的 胎儿水动力学和血容量的改变。尽管 母体复水、胎儿内分泌和体液反应持续存在 超越基础母体和胎儿血浆OSM的回归。作为一名 结果,发作性母体脱水可能导致 羊水过少、早产和/或胎儿的发展 发育迟缓。该项目将长期利用 用插管绵羊模型研究胎儿和胎儿的个体发育 母体对羊水和电解质的反应 脱水和随后的复水。区隔模型将 用来量化胎儿积水的变化 (胎儿吞咽和经胎盘流动)和排泄(尿液和 肺液)。具体地说,我们已经制定并确认了一项 胎儿吞咽活动和吞咽容量的测量方法 胎儿尿液和肺液产量将直接测量, 并计算了胎盘血流量。由此产生的对胎儿的影响 出血量及其对羊水和尿囊水的影响 将对车厢进行评估。精选胎儿的反应 将对水的动态平衡的核心内分泌系统进行检查,并 胎儿体液的内分泌调节机制及临床意义 电解质和吞咽反应的研究将使用 选择性激动剂和拮抗剂。作为母体和胎儿 对再水化的反应因模式不同而不同 水化,这个项目还将检查胎儿的内分泌和 对几种母体补液方式的体液反应。研究 绵羊模型的脱水和复水代表一种 为了解母子水动力学提供了一种有希望的方法, 在解决围产期潜在的关键问题时 医药。

项目成果

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Michael Glenn Ross其他文献

Michael Glenn Ross的其他文献

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{{ truncateString('Michael Glenn Ross', 18)}}的其他基金

Mechanisms of Programmed Gestational Hyperphagia
程序性妊娠期食欲过盛的机制
  • 批准号:
    7614207
  • 财政年份:
    2008
  • 资助金额:
    $ 12.64万
  • 项目类别:
Mechanisms of Programmed Gestational Hyperphagia
程序性妊娠期食欲过盛的机制
  • 批准号:
    7467418
  • 财政年份:
    2008
  • 资助金额:
    $ 12.64万
  • 项目类别:
Mechanisms of Programmed Gestational Hyperphagia
程序性妊娠期食欲过盛的机制
  • 批准号:
    7799747
  • 财政年份:
    2008
  • 资助金额:
    $ 12.64万
  • 项目类别:
Mechanisms of Programmed Gestational Hyperphagia
程序性妊娠期食欲过盛的机制
  • 批准号:
    8250374
  • 财政年份:
    2008
  • 资助金额:
    $ 12.64万
  • 项目类别:
Mechanisms of Programmed Gestational Hyperphagia
程序性妊娠期食欲过盛的机制
  • 批准号:
    8052762
  • 财政年份:
    2008
  • 资助金额:
    $ 12.64万
  • 项目类别:
DO IONIZED MAGNESIUM LEVELS PREDICT CLINICAL EFFECTS BETTER THAN TOTAL MAGNESIS
离子镁水平比总镁水平更能预测临床效果吗
  • 批准号:
    7606211
  • 财政年份:
    2007
  • 资助金额:
    $ 12.64万
  • 项目类别:
AQUAPORIN GENE EXPRESSION IN HUMAN FETAL MEMBRANE
人胎膜中水通道蛋白基因的表达
  • 批准号:
    7606210
  • 财政年份:
    2007
  • 资助金额:
    $ 12.64万
  • 项目类别:
AQUAPORIN GENE EXPRESSION IN HUMAN FETAL MEMBRANE
人胎膜中水通道蛋白基因的表达
  • 批准号:
    7376108
  • 财政年份:
    2005
  • 资助金额:
    $ 12.64万
  • 项目类别:
THE COMPARISON OF PLACENTAL AND UMBILICAL NUCLEATED RED BLOOD CELL COUNT
胎盘和脐带有核红细胞计数的比较
  • 批准号:
    7376109
  • 财政年份:
    2005
  • 资助金额:
    $ 12.64万
  • 项目类别:
THE COMPARISON OF PLACENTAL AND UMBILICAL NUCLEATED RED BLOOD CELL COUNT
胎盘和脐带有核红细胞计数的比较
  • 批准号:
    7206410
  • 财政年份:
    2004
  • 资助金额:
    $ 12.64万
  • 项目类别:

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精氨酸加压素的 PET 配体发现
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Role of arginine-vasopressin and V1A receptor in psychosocial stress-induced myocardial injury
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  • 批准号:
    10283131
  • 财政年份:
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Role of arginine-vasopressin and V1A receptor in psychosocial stress-induced myocardial injury
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    10470346
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RGC 释放的精氨酸加压素对昼夜节律和精神功能的生理作用
  • 批准号:
    19K06939
  • 财政年份:
    2019
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    Grant-in-Aid for Scientific Research (C)
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精氨酸加压素受体 1A 在周围神经病理性疼痛中的作用机制的鉴定
  • 批准号:
    18K16609
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Functional mapping of arginine vasopressin receptor 1A circuits that promote anorexic behavior
促进厌食行为的精氨酸加压素受体 1A 电路的功能图谱
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Usefulness of arginine vasopressin levels on admission in risk stratification of acute decompensated heart failure with preserved left ventricular ejection fraction
入院时精氨酸加压素水平在左心室射血分数保留的急性失代偿性心力衰竭风险分层中的作用
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    16K09448
  • 财政年份:
    2016
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Variation in the arginine vasopressin 1a receptor (AVPR1a) gene, the social environment, general health and wellbeing
精氨酸加压素 1a 受体 (AVPR1a) 基因的变异、社会环境、总体健康和福祉
  • 批准号:
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  • 财政年份:
    2013
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    $ 12.64万
  • 项目类别:
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