Buhimschi I, Yallampalli C, Dong Y L, Garfield R E
Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, USA.
Am J Obstet Gynecol. 1995 May;172(5):1577-84. doi: 10.1016/0002-9378(95)90500-6.
The aims of the study were to investigate whether a nitric oxide-cyclic guanosine monophosphate relaxation pathway is present in the human uterus and whether it differentially inhibits contractility during pregnancy and labor.
Myometrial strips were obtained from pregnant women who were either in labor or not in labor and from nonpregnant women. Nitrites and cyclic guanosine monophosphate production by the tissues and contractile responses to nitric oxide modifiers were measured.
Biochemical assays revealed that nitric oxide (nitrites) and cyclic guanosine monophosphate are generated by the human uterus. Cyclic guanosine monophosphate production by the uterus was increased by L-arginine (the substrate for nitric oxide) and diethylamine/nitric oxide (a nitric oxide donor) and decreased by nitro-L-arginine methyl ester (an inhibitor of nitric oxide synthase). Spontaneous contractility in vitro was increased by nitro-L-arginine methyl ester and decreased by diethylamine/nitric oxide, which furthermore produced a dose-dependent inhibition of contractility, and the median effective dose of inhibition in tissues from nonlaboring pregnant patients (1.5 +/- 0.4 mumol/L) is substantially lower than in tissues from laboring pregnant (21.7 +/- 7.4 mumol/L or nonpregnant (20.8 +/- 4.4 mumol/L) women. These studies show that the nitric oxide-cyclic guanosine monophosphate system exists in the human uterus and that it inhibits contractility. Furthermore, the relaxation responsiveness to nitric oxide is elevated during pregnancy and decreased during labor.
A nitric oxide-cyclic guanosine monophosphate relaxation pathway is present in the human uterus and may be responsible for maintaining uterine quiescence during pregnancy. A decrease in uterine relaxation responsiveness to nitric oxide at term may play a role in the initiation of labor.
本研究旨在调查一氧化氮 - 环磷酸鸟苷舒张途径是否存在于人体子宫中，以及它在妊娠和分娩期间对子宫收缩的抑制作用是否存在差异。
从正在分娩或未分娩的孕妇以及未孕女性获取子宫肌条。测量组织中亚硝酸盐和环磷酸鸟苷的生成量以及对一氧化氮调节剂的收缩反应。
生化分析显示人体子宫可生成一氧化氮（亚硝酸盐）和环磷酸鸟苷。L - 精氨酸（一氧化氮的底物）和二乙胺/一氧化氮（一氧化氮供体）可增加子宫中环磷酸鸟苷的生成量，而硝基 - L - 精氨酸甲酯（一氧化氮合酶抑制剂）则使其减少。体外自发收缩性在加入硝基 - L - 精氨酸甲酯后增强，加入二乙胺/一氧化氮后减弱，且二乙胺/一氧化氮对收缩性产生剂量依赖性抑制，未分娩孕妇组织中的半数有效抑制剂量（1.5±0.4μmol/L）显著低于分娩孕妇组织（21.7±7.4μmol/L）或未孕女性组织（20.8±4.4μmol/L）。这些研究表明人体子宫中存在一氧化氮 - 环磷酸鸟苷系统，且该系统可抑制子宫收缩。此外，妊娠期间对一氧化氮的舒张反应性升高，分娩期间降低。
人体子宫中存在一氧化氮 - 环磷酸鸟苷舒张途径，可能负责维持妊娠期间子宫的静息状态。足月时子宫对一氧化氮舒张反应性的降低可能在分娩发动中起作用。
