Quaas L, Göppinger A, Zahradnik H P
Department of Obstetrics and Gynecology, University of Freiburg, F.R.G.
Prostaglandins. 1987 Aug;34(2):257-69. doi: 10.1016/0090-6980(87)90248-6.
The effects of acetylsalicylic acid (ASA) and indomethacin (IND) on the epinephrine and oxytocin stimulated contractility and prostaglandin (6-keto-PGF1 alpha, PGF2 alpha) production of superfused myometrial strips from the pregnant human uterus at term are reported. Without preincubation in ASA or IND epinephrine dose-dependently (10 ng/ml to 1 microgram/ml) stimulated the contractility and significantly increased the PG-release of the myometrial strips. The epinephrine induced increase in contractility was correlated to a higher increase in PGF2a production and a decreased 6-keto-PGF1 alpha/PGF2 alpha ratio (5.4 to 1.8). Superfusion of oxytocin increased myometrial contractions and PGF2 alpha release according to dose (3-12 microU/ml). However, 6-keto-PGF1 alpha production was not affected by oxytocin. Myometrial strips preincubated with ASA (100 micrograms/ml) or IND (10 micrograms/ml) demonstrated little spontaneous activity and the PG production was below the detection limit of the RIA. The stimulating effect of epinephrine and oxytocin on the contractility and PGF2 alpha release of the myometrial strips was inhibited significantly. During continuous superfusion of the ASA and IND preincubated myometrial strips with Tyrode's solution the inhibitory effect on spontaneous, epinephrine-, and oxytocin-stimulated contractility and PGF2 alpha release gradually declined over a period of 2 hours. This decrease of the inhibitory effect was more significant in ASA preincubated specimens. Our results demonstrate that spontaneous, epinephrine-, and oxytocin-stimulated contractility and PG release of human myometrial strips can be inhibited by ASA and IND and that this inhibitory effect is reversible. Furthermore our results suggest that in pregnant human myometrium the inhibition of PGF2 alpha production by ASA and IND is more pronounced than that of 6-keto-PGF1 alpha (PGI2).
本文报道了乙酰水杨酸(ASA)和吲哚美辛(IND)对足月妊娠人子宫超融合肌层条带中肾上腺素和催产素刺激的收缩性以及前列腺素(6-酮-前列腺素F1α、前列腺素F2α)生成的影响。在未用ASA或IND预孵育的情况下,肾上腺素剂量依赖性地(10 ng/ml至1 μg/ml)刺激肌层条带的收缩性,并显著增加其前列腺素释放。肾上腺素诱导的收缩性增加与前列腺素F2α生成的更高增加以及6-酮-前列腺素F1α/前列腺素F2α比值降低(从5.4降至1.8)相关。催产素超融合根据剂量(3 - 12 μU/ml)增加肌层收缩和前列腺素F2α释放。然而,6-酮-前列腺素F1α生成不受催产素影响。用ASA(100 μg/ml)或IND(10 μg/ml)预孵育的肌层条带显示出很少的自发活性,且前列腺素生成低于放射免疫分析的检测限。肾上腺素和催产素对肌层条带收缩性和前列腺素F2α释放的刺激作用被显著抑制。在用台氏液持续超融合ASA和IND预孵育的肌层条带期间,对自发、肾上腺素和催产素刺激的收缩性以及前列腺素F2α释放的抑制作用在2小时内逐渐下降。这种抑制作用的降低在ASA预孵育的标本中更为显著。我们的结果表明,ASA和IND可抑制人肌层条带的自发、肾上腺素和催产素刺激的收缩性及前列腺素释放,且这种抑制作用是可逆的。此外,我们的结果表明,在妊娠人子宫肌层中,ASA和IND对前列腺素F2α生成的抑制比对6-酮-前列腺素F1α(前列环素)更为明显。