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ARACHIDONIC ACID METABOLITES AND UTERINE CONTRACTIONS

ARACHIDONIC ACID METABOLITES AND UTERINE CONTRACTIONS
花生四烯酸代谢物和子宫收缩
批准号:
3319251
负责人:
W Y CHAN
金额:
$15.57万
依托单位国家:
美国
项目类别:
财政年份:
1986
资助国家:
美国
项目状态:
已结题
起止时间:
1986-01-01 至 1989-06-30

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中文摘要
翻译
本项目的长期目标是阐明 子宫收缩中的前列腺素(PGs)和催产素(OT), 特别是在分娩和早产中。 有两个具体目标 在拟议的项目中。 1.探讨前列腺素类药物在OT发病中的作用机制 分娩子宫的敏感性。 妊娠期子宫发育 对催产素的子宫收缩作用明显敏感。 抑制 内源性PG合成阻止OT敏感性的发展。 的 PG对OT的这种作用机制尚不清楚。 了解PG如何 刺激OT敏感性是我们了解其机制的基础 分娩和我们的研究有效的治疗方法, 早产 可以想象,PG可以刺激OT受体和/或间隙, 连接形成,从而增强OT的作用。 我们将确定 在第19、20、21和24天, 22只妊娠和产后第2天大鼠子宫肌层OT受体 浓度和间隙连接形成。 OT受体浓度将 通过经典的配体-受体结合和Scathard图确定 分析. 间隙连接的形成将通过以下方法定量测量: 电镜 2.为了测定白三烯(LT)和PG的产生以及子宫内膜的 免疫致敏大鼠或豚鼠的收缩性。 在 除了前列腺素外,子宫还合成LT。 LT的功能, 子宫还没有被探查过 LT和PG是 炎症和超敏反应。 前列腺素类如LT, 在妊娠期间,PFG-2 α、TXA-2可能在妊娠子宫中显著升高。 感染、炎症或超敏反应,产生 收缩和血管变化与胎儿生长不相容。 这 机制可能是负责,在某些情况下,流产或自发 堕胎 我们建议测定LTs、PGE-2、PGF-2的产生, 子宫收缩力与α、PGI-2、TXA-2的关系 致敏大鼠或豚鼠。 动物将被主动致敏, 卵清蛋白。 子宫收缩和前列腺素类的释放将 在抗原攻击下测定。 组织内容物和释放 前列腺素类将通过放射免疫测定和生物测定来测量。
英文摘要
The long-term objective of this project is to elucidate the role of prostaglandins (PGs) and oxytocin (OT) in uterine contractions, particularly in parturition and preterm labor. There are two specific aims in the proposed project. 1. To investigate the mechanism of action of PGs on the development of OT sensitivity in the parturient uterus. The pregnant uterus at term develops a marked sensitivity to the uterotonic action of OT. Inhibition of endogenous PG synthesis prevents the development of OT sensitivity. The mechanism of this action of PG on OT is not known. Understanding how PG stimulates OT sensitivity is fundamental to our knowledge of the mechanism of parturition and to our research for effective treatment methods for preterm labor. Conceivably, PGs may stimulate OT receptor and/or gap junction formations and thus enhance the action of OT. We will determine the effects of inhibition of endogenous PG synthesis in day 19, 20, 21 and 22 pregnant and day 2 postpartum rats on myometrial OT receptor concentrations and gap junction formations. OT receptor concentration will be determined by classical ligand-receptor binding and Scathard plot analysis. Gap junction formations will be measured quantitatively by electron microscopy. 2. To determine leukotrienes (LTs) and PG production and uterine contractility in immunologically sensitized rats or guinea pigs. In addition to PGs, the uterus also synthesizes LTs. The functions of LTs in the uterus has not been explored. LTs and PGs are mediators of inflammatory and hypersensitivity reactions. Prostanoids such as LTs, PFG-2 alpha, TXA-2 may be greatly elevated in the pregnant uterus during infection, inflammatory or hypersensitivity reactions, producing contractions and vascular changes incompatible to fetal growth. This mechanism may be responsible, in some cases, for miscarriage or spontaneous abortion. We propose to determine the production of LTs, PGE-2, PGF-2 Alpha, PGI-2 and TXA-2 and uterine contractility in immunologically sensitized rats or guinea pigs. Animals will be actively sensitized with ovalbumin. Uterine contractions and release of prostanoids will be determined under antigen challenge. Tissue contents and release of prostanoids will be measured by radioimmunoassays and bioassays.
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ARACHIDONIC ACID METABOLITES AND UTERINE CONTRACTIONS
ARACHIDONIC ACID METABOLITES AND UTERINE CONTRACTIONS
ARACHIDONIC ACID METABOLITES AND UTERINE CONTRACTIONS
ARACHIDONIC ACID METABOLITES AND UTERINE CONTRACTIONS
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