Giussani D A, Jenkins S L, Mecenas C A, Winter J A, Barbera M, Honnebier O M, Nathanielsz P W
Laboratory for Pregnancy and Newborn Research, Cornell University College of Veterinary Medicine, Ithaca, New York 14853-6401, USA.
Endocrinology. 1996 Aug;137(8):3302-7. doi: 10.1210/endo.137.8.8754755.
We tested the hypothesis that increased oxytocin is a necessary mechanism for the mediation of androstenedione (delta 4A)-induced myometrial contractions by investigating the effects of maternal treatment with the oxytocin antagonist atosiban on in vivo delta 4A-induced contractions. In four monkeys (group I), maternal estradiol, oxytocin, and myometrial contractions were assessed at baseline and after continuous iv delta 4A administration. Similar measurements were made in three monkeys (group II) that received the same delta 4A infusion regimen, but in addition were treated daily with atosiban. Maternal estradiol and oxytocin levels and contractions were also assessed in four additional monkeys (controls; group III), in which the delta 4A vehicle, intralipid, was infused iv continuously. In group I, delta 4A induced myometrial contractions and increased maternal estradiol and oxytocin to term concentrations. No myometrial contractions occurred in group II monkeys after combined delta 4A and atosiban treatment despite estradiol being elevated to concentrations similar to those measured in group I monkeys. Atosiban had no effect on maternal heart rate or blood pressure. Maternal estradiol, oxytocin, and number of myometrial contractions remained unchanged from baseline values in control monkeys. In conclusion, oxytocin is a necessary part of the mechanisms mediating delta 4A-induced myometrial contractions. delta 4A promotes myometrial contractions via similar mechanisms that mediate spontaneous term contractions in pregnant monkeys.
我们通过研究用催产素拮抗剂阿托西班对母体进行治疗对体内雄烯二酮（δ4A）诱导的子宫收缩的影响，来检验以下假设：催产素增加是介导δ4A诱导子宫肌层收缩的必要机制。在4只猴子（第一组）中，在基线以及持续静脉注射δ4A后，评估母体雌二醇、催产素和子宫肌层收缩情况。在另外3只猴子（第二组）中进行了类似测量，它们接受相同的δ4A输注方案，但除此之外每天还用阿托西班进行治疗。另外4只猴子（对照组；第三组）持续静脉输注δ4A载体脂质乳剂，也对其母体雌二醇、催产素水平及子宫收缩情况进行了评估。在第一组中，δ4A诱导子宫肌层收缩，并使母体雌二醇和催产素升高至足月浓度。在第二组猴子中，联合给予δ4A和阿托西班治疗后未出现子宫肌层收缩，尽管雌二醇升高至与第一组猴子测得的浓度相似。阿托西班对母体心率或血压无影响。对照组猴子的母体雌二醇、催产素及子宫肌层收缩次数与基线值相比无变化。总之，催产素是介导δ4A诱导子宫肌层收缩机制的必要组成部分。δ4A通过与介导妊娠猴子自发性足月收缩相似的机制促进子宫肌层收缩。
