The roles of nitric oxide and prostaglandins in myometrium at proterm

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通路。一氧化氮在妊娠中期抑制大鼠子宫的自发收缩，但在足月时没有，显示出胎龄依赖性抑制。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作用，但硝酸甘油则不然，硝酸甘油需要代谢转化才能释放一氧化氮。临近或足月时对一氧化氮的难耐性与胎盘组织的存在与否无关。妊娠22 ~ 26周血浆NO代谢物浓度显著高于未妊娠妇女，但妊娠后期血浆NO代谢物浓度略有下降。早产患者血浆NO代谢物浓度低于同周正常孕妇。这些研究表明NO在维持妊娠中期子宫静止中起重要作用。足月子宫对NO的松弛反应减少可能在分娩开始中起作用。此外，LPS可以减弱NO对收缩的抑制作用。妊娠中期感染的子宫肌层似乎比妊娠后期正常子宫肌层对收缩的敏感性增加。胎盘因子对一氧化氮抑制收缩的作用减弱，不依赖于一氧化氮在子宫中的作用。绒毛膜炎可能通过不依赖于一氧化氮的机制导致早产。

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.