Dong Y L, Dai B S, Singh P, Yallampalli C
Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, USA.
Am J Obstet Gynecol. 1997 Oct;177(4):907-17. doi: 10.1016/s0002-9378(97)70293-x.
Our purpose was to investigate the roles of nitric oxide and prostaglandins in controlling parturition.
Pregnant rats on day 18 of gestation were injected intraperitoneally with prostaglandin F2 alpha, prostaglandin F2 alpha plus diethylenetriamine-nitric oxide (a donor of nitric oxide), prostaglandin F2 alpha plus diethylenetriamine without nitric oxide, or vehicle. Uterine nitrite production, nitric oxide synthase messenger ribonucleic acid and contractile response in vitro, and serum progesterone levels were measured. The labor and delivery of the rats also were monitored.
Exogenously administered prostaglandin F2 alpha significantly inhibited nitric oxide production by the uterus in a time-dependent manner with maximal effects observed 48 hours after prostaglandin F2 alpha treatment. Messenger ribonucleic acid for inducible nitric oxide synthase but not endothelial nitric oxide synthase messenger ribonucleic acid in the uterus was significantly inhibited by prostaglandin F2 alpha with maximal inhibition at 48 hours after prostaglandin F2 alpha injection. The serum progesterone concentration was substantially reduced by prostaglandin F2 alpha, and this reduction was partially reversed by administration of diethylenetriamine-nitric oxide but not diethylenetriamine without nitric oxide. Prostaglandin F2 alpha caused increases in contractile activity of the uterus in a dose-dependent manner. Diethylenetriamine-nitric oxide (10(-4) mol/L) blocked prostaglandin F2 alpha-induced contractions. Premature parturition was induced within 48 hours after prostaglandin F2 alpha injection in 100% of the animals. Coadministration of diethylenetriamine-nitric oxide completely prevented the preterm labor induced by prostaglandin F2 alpha.
Prostaglandin F2 alpha inhibited inducible nitric oxide synthase messenger ribonucleic acid and subsequent nitric oxide generation in the rat uterus. Nitric oxide can prevent prostaglandin F2 alpha-induced preterm labor, possibly by attenuating the fall in serum progesterone and blocking uterine contractions induced by prostaglandin F2 alpha administration.
我们的目的是研究一氧化氮和前列腺素在控制分娩中的作用。
在妊娠第18天的怀孕大鼠腹腔注射前列腺素F2α、前列腺素F2α加二乙烯三胺 - 一氧化氮（一氧化氮供体）、前列腺素F2α加不含一氧化氮的二乙烯三胺或赋形剂。测量子宫亚硝酸盐生成、一氧化氮合酶信使核糖核酸和体外收缩反应以及血清孕酮水平。还监测大鼠的分娩情况。
外源性给予前列腺素F2α以时间依赖性方式显著抑制子宫一氧化氮生成，在前列腺素F2α治疗后48小时观察到最大效应。前列腺素F2α显著抑制子宫中诱导型一氧化氮合酶的信使核糖核酸，但不抑制内皮型一氧化氮合酶信使核糖核酸，在前列腺素F2α注射后48小时抑制作用最大。前列腺素F2α使血清孕酮浓度大幅降低，给予二乙烯三胺 - 一氧化氮可部分逆转这种降低，但给予不含一氧化氮的二乙烯三胺则不能。前列腺素F2α以剂量依赖性方式引起子宫收缩活性增加。二乙烯三胺 - 一氧化氮（10⁻⁴mol/L）可阻断前列腺素F2α诱导的收缩。在前列腺素F2α注射后48小时内，100%的动物发生早产。联合给予二乙烯三胺 - 一氧化氮可完全预防前列腺素F2α诱导的早产。
前列腺素F2α抑制大鼠子宫中诱导型一氧化氮合酶信使核糖核酸及随后的一氧化氮生成。一氧化氮可预防前列腺素F2α诱导的早产，可能是通过减轻血清孕酮下降以及阻断前列腺素F2α给药诱导的子宫收缩来实现。
