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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
这个项目的长期目标是阐明 前列腺素(PGs)和催产素(OT)与子宫收缩 特别是在分娩和早产方面。有两个明确的目标 在拟议的项目中。 1.探讨前列腺素在OT发病中的作用机制 临产时子宫的敏感性。怀孕的子宫在足月发育 对催产素的强宫作用有明显的敏感性。抑制 内源性PG合成可阻止OT敏感性的发展。这个 PG对OT的这种作用机制尚不清楚。了解PG如何 刺激OT敏感性是我们了解该机制的基础 以及我们对有效的治疗方法的研究 早产。可想而知,PGs可能刺激OT受体和/或GAP 形成连接,从而增强OT的作用。我们将决定 内源性PG合成抑制在第19、20、21、21天的作用 22只孕鼠和产后第2天子宫肌层OT受体的研究 浓度和缝隙连接的形成。OT受体浓度将 由经典配基-受体结合图和Sexusard图确定 分析。缝隙连接的形成将通过以下方式进行定量测量 电子显微镜。 2.测定白三烯(LTS)和前列腺素(PG)的产生及子宫 免疫致敏大鼠或豚鼠的收缩能力。在……里面 除了前列腺素,子宫还合成LT。LTS在中的作用 子宫还没有被探查过。LTS和PGS是 炎症和过敏性反应。前列腺素类物质,如LTS, Pfg-2α、TXA-2在妊娠子宫中可能显著升高 感染、炎症或过敏性反应,产生 宫缩和血管变化与胎儿生长不相容。这 在某些情况下,机制可能是流产或自发流产的原因 堕胎。我们建议确定LTS、PGE-2、PGF-2的产量 免疫学中α、PGI-2、TXA-2与子宫收缩功能的关系 致敏大鼠或豚鼠。动物将被积极地致敏 卵清蛋白。子宫收缩和前列腺素释放将 在抗原挑战下确定的。组织中的含量和释放 前列腺素将通过放射免疫测定法和生物测定法进行测定。
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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