1979 年 99 巻 1 号 p. 14-19
The rate of release of prostaglandin F2α (PGF2α) from isolated rat uterus increased markedly from 18 to 21 days of pregnancy. During parturition, it still maintained a high level. When 2-(2-fluoro-4-biphenylyl) propionic acid (flurbiprofen) and indomethacin were orally administered, 0.5 and 2.5 mg/kg twice a day, to pregnant rats from 18th day of gestation to the begining of parturition, the rate of release of PGF2α from the uterus at the time of parturition was reduced by both anti-inflammatory agents. The ability to inhibit the release of PGF2α was more intense in flurbiprofen than in indomethacin in conformity with the results of prolonged pregnancy and delayed spontaneous delivery induced by these drugs. PGF2α level in peripheral plasma increased significantly at the time of parturition. Flurbiprofen and indomethacin were also found to hinder the rise in PGF2α level. 17β-Estradiol in plasma gradually increased in late pregnancy, whereas progesterone in plasma rapidly decreased on 21st day. Neither flurbiprofen nor indomethacin exerted any effect on the action of 17β-estradiol. The drop of progesterone during parturition was hindered relatively little by both drugs. Furthermore, regression of the corpora lutea during parturition was obviously inhibited by both drugs. However, 20α-hydroxysteroid dehydrogenase activity in the corpora lutea was not affected. Δ5-Isomerase activity was enhanced only by flurbiprofen. These results indicated that deficiency of PGF2α release in the uterus might result in the delay of spontaneous derivery, and also concomitant inhibition of luteolysis might be involved in the prolongation of pregnancy induced by treatment with these anti-inflammatory agents.