Ramondt J, Verhoeff A, Garfield R E, Wallenburg H C
Department of Obstetrics and Gynecology, Erasmus University School of Medicine and Health Sciences, Rotterdam, The Netherlands.
Eur J Obstet Gynecol Reprod Biol. 1994 Mar 31;54(1):63-9. doi: 10.1016/0028-2243(94)90082-5.
The objective was to elucidate the functional relationship between estradiol-induced changes in myometrial activity, uterine prostanoid synthesis, and gap junction formation in vivo. The study design was as follows. The effects of inhibition of prostanoid synthesis with naproxen on formation of gap junctions and coordination of electrical and mechanical myometrial activity induced by estradiol-17 beta were investigated in 6 chronically instrumented oophorectomized ewes. Prostanoid metabolites were measured in arterial and uterine venous plasma. Myometrial biopsies were obtained to determine gap junction area. The results were that intraarterial administration of 0.1 mg of estradiol-17 beta was followed by a significant increase in maximum rate of rise of the intrauterine pressure cycles and a significant decrease in conduction time of bursts of electrical activity; this response was not altered by pharmacologic inhibition of uterine prostanoid synthesis using naproxen. Estradiol administration during continuous naproxen infusion increased gap junction area. The conclusion is that improved coordination of myometrial activity and formation of myometrial gap junctions induced by estradiol is not mediated by prostaglandins.
目的是阐明雌二醇诱导的子宫肌层活动变化、子宫前列腺素合成与体内缝隙连接形成之间的功能关系。研究设计如下。在6只长期植入仪器的去卵巢母羊中,研究了用萘普生抑制前列腺素合成对缝隙连接形成以及由17β - 雌二醇诱导的子宫肌层电活动和机械活动协调性的影响。在动脉血浆和子宫静脉血浆中测量前列腺素代谢产物。获取子宫肌层活检样本以确定缝隙连接面积。结果是,动脉内注射0.1mg的17β - 雌二醇后,子宫内压力周期的最大上升速率显著增加,电活动爆发的传导时间显著缩短;使用萘普生对子宫前列腺素合成进行药理抑制并未改变这种反应。在持续输注萘普生期间给予雌二醇可增加缝隙连接面积。结论是,雌二醇诱导的子宫肌层活动协调性改善和子宫肌层缝隙连接形成不是由前列腺素介导的。