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The roles of nitric oxide and prostaglandins in myometrium at proterm

一氧化氮和前列腺素在早产儿子宫肌层中的作用

基本信息

批准号：
12671619
负责人：
OKAWA Toshiaki
金额：
$ 0.9万
依托单位：
Fukushima Medical University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2000
资助国家：
日本
起止时间：
2000 至 2002
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-12671619/
关键词：
NO Prostaglandin Myometrium LPS NOx preterm birth NO donor Nitric Oxide prostaglandins 子宮筋収縮 Endotoxin インターロイキン-1 nitric oxide prostaglandin Prostaglandin

项目摘要

We demonstrated that an L-arginine-NOL-cGMP pathway exists in pregnant rat uterus, through in vitro and in vivo experiments. Nitric oxide inhibits spontaneous contractions in rat uterus at midgestation but not at term, demonstrating gestational age-dependent inhibition. The presence of placental tissue enhances inhibition of uterine contractility by agents that spontaneously release nitric oxide, such as diethylamine-nitric oxide, but not by nitroglycerin, which requires metabolic transformation for nitric oxide to be released. Refractoriness to nitric oxide near or at term does not depend on the presence or absence of placental tissue.The plasma NO metabolite concentration in 22-26 weeks of pregnancy was significantly higher than that of the non pregnant women, although the plasma NO nietabolite concentration was slightly decreased toward term. The plasma NO metabolite concentration in patients with preterm labor was lower than that of the normal pregnant women in same weeks of pregnancy.These studies suggest that NO has an important role in maintaining uterine quiescence at midgestation. A decrease in uterine relaxation responsiveness to NO at term may play a role in the initiation of labor. Furthermore, LPS attenuated the inhibition of contraction by NO. Myometrium with infection at midgestation seems to increase sensitivity to contractility compared to normal myometrium at late gestation. Effect of placental factor which is attenuated on inhibition of contractions by NO did not depend on iNOS in uterus Chorioaminionitis might induce preterm labor via an iNOS-independent mechanism.

我们通过体外和体内实验证明了妊娠大鼠子宫中存在L-精氨酸-NOL-cGMP通路。一氧化氮抑制大鼠妊娠中期子宫的自发性收缩，但不抑制足月子宫的自发性收缩，表明具有孕龄依赖性抑制作用。胎盘组织的存在增强了自发释放一氧化氮的药物（如二乙胺-一氧化氮）对子宫收缩力的抑制，但不增强硝酸甘油对子宫收缩力的抑制，硝酸甘油需要代谢转化才能释放一氧化氮。妊娠22-26周血浆NO代谢产物浓度明显高于非妊娠妇女，但随着妊娠的进行，血浆NO代谢产物浓度略有下降。早产患者血浆NO代谢产物浓度低于同孕周正常孕妇，提示NO在维持妊娠中期子宫静止中起重要作用。足月时子宫对NO的舒张反应性降低可能在分娩的开始中起作用。此外，LPS减弱了NO对收缩的抑制作用。妊娠中期感染的子宫肌层与妊娠晚期正常子宫肌层相比，似乎增加了对收缩的敏感性。胎盘因子对NO抑制子宫收缩的作用减弱，其作用不依赖于iNOS。绒毛膜羊膜炎可能通过一种不依赖iNOS的机制诱发早产。