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The role of nitric oxide on uterine contraction at preterm

一氧化氮对早产子宫收缩的作用

基本信息

批准号：
10671560
负责人：
OKAWA Toshiaki
金额：
$ 2.05万
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：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10671560/
关键词：
NO.uterus uterine contraction NOx K ca channel NO denor placento preterm birth 子宮筋 NOドナーラット Nitric Oxide (NO)妊娠血清 NO代謝産物

项目摘要

We demonstrated that an L-arginine-NO-cGMP pathway exists in pregnant rat uterus, through in vitro and in vivo experiments. Nitric oxide inhibits spontaneous contractions in rate uterus at midgestation but not at term, demonstrating gestational age-dependent inhibition. There is gestational age-dependent refractoriness to calcium-dependent potassium but not adenosine triphosphate-dependent potassium channel opener-induced inhibition of spontaneous contractile activity of isolated rat uterine rings. Nitric oxide inhibits uterine contractions by opening of calcium-dependent potassium channels in pregnant rat myometrium. Refractoriness to nitric oxide toward term may result from decreased probability to open or number of calcium-dependent potassium channels. The presence of placental tissue enhances inhibition of uterine contractility by agents that spontaneously release nitric oxide, such as diethylamine-nitric oxide, but no 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 metabolite 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. Therefore, decreasing NO products may be one of the causes of preterm birth.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. Nitric oxide donor drugs may be very effective in suppressing preterm labor.

我们通过体外和体内实验证明，妊娠大鼠子宫中存在L-精氨酸-NO-cGMP途径。一氧化氮在妊娠中期抑制子宫自发收缩，但在足月时不抑制，表现出孕龄依赖性抑制。钙依赖性钾通道开放剂对钙依赖性钾离子的抑制作用与胎龄有关，但三磷酸腺苷依赖性钾通道开放剂对大鼠子宫环自发收缩活动的抑制作用不明显。一氧化氮通过开放妊娠大鼠子宫肌层钙依赖性钾通道来抑制子宫收缩。一氧化氮对终末期的不耐受可能是由于钙依赖钾通道开放的概率或数量减少所致。胎盘组织的存在加强了对子宫收缩的抑制，这些药物自发释放一氧化氮，如二乙胺-一氧化氮，但不能通过硝酸甘油，这需要代谢转换来释放一氧化氮。妊娠22~26周时血浆NO代谢产物浓度显著高于未孕妇女，而足月时血浆NO代谢产物浓度略有下降。早产患者的血浆NO代谢产物浓度低于正常妊娠妇女。因此，NO产物的减少可能是早产的原因之一。这些研究表明，NO在维持中期子宫静止中起着重要作用。足月子宫松弛对NO的反应性降低可能在分娩的开始过程中起作用。一氧化氮供体药物在抑制早产方面可能非常有效。