Ruddock Nicole K, Shi Shao-Qing, Jain Sangeeta, Moore Gradie, Hankins Gary D V, Romero Roberto, Garfield Robert E
Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, TX, USA.
Am J Obstet Gynecol. 2008 Oct;199(4):391.e1-7. doi: 10.1016/j.ajog.2008.06.085.
The aim was to determine whether progesterone (P4) or 17-alpha-hydroxyprogesterone caproate (17P) directly inhibit human uterine contractility in vitro and thereby clarify their mechanisms of action.
Myometrial tissues were suspended in organ chambers and exposed for 2 to 20 hours to varying concentrations of P4 or 17P or solvent. Contractile activity was registered, stored, and analyzed. Dose response curves were then generated for P4 or 17P at various times.
P4 significantly inhibited spontaneous contractility dose dependently. The inhibition was not blocked by RU486 but was reversible after washing. Surprisingly, 17P dose dependently stimulated contractility. HPLC and GC-MS methods were used to determine the detectable concentrations of progestins in the baths.
P4, at concentrations equivalent to those present in the placenta and uterus, inhibit spontaneous myometrial contractility in vitro by nongenomic mechanisms.
旨在确定孕酮(P4)或己酸17α-羟孕酮(17P)是否在体外直接抑制人子宫收缩力,从而阐明其作用机制。
将子宫肌层组织悬于器官浴槽中,使其暴露于不同浓度的P4或17P或溶剂中2至20小时。记录、存储并分析收缩活性。然后在不同时间生成P4或17P的剂量反应曲线。
P4显著剂量依赖性地抑制自发收缩力。该抑制作用未被RU486阻断,但冲洗后可逆。令人惊讶的是,17P剂量依赖性地刺激收缩力。采用高效液相色谱法和气相色谱-质谱法测定浴槽中可检测到的孕激素浓度。
在相当于胎盘和子宫中存在的浓度下,P4通过非基因组机制在体外抑制子宫肌层自发收缩力。