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We have tested the action of a catechol oestrogen -2,3,17 beta-trihydroxy oestra-1,3,5 (10)-triene (2-OH oestradiol) in stimulating prostaglandin (PG) production by an homogenate of rat uterus. Marked and dose dependent stimulation was observed in PGF2 alpha and PGE2 production using 20-250 microM concentrations of catechol oestrogen; a concentration of 250 microM 2-OH oestradiol resulted in a 23 fold increase in PGF2 alpha production with a 50% reduction in the synthesis of 6-keto PGF1 alpha. Tryptophan, catechol and glutathione were without effect on PGF2 alpha and PGE2 production whereas adrenalin stimulated the production of all PGs, although the increase was less than that seen with 2-OH oestradiol. Oestradiol had a slight stimulatory action on PGF2 alpha production which reached a maximum at around 40 microM but had a more marked stimulation of 6-keto PGF1 alpha formation. Stimulation of prostaglandin production by oestradiol and 2-OH oestradiol showed no variation at different stages of the rat oestrous cycle. The use of 5 to 100 mg of tissue/ml gave similar product distribution although the effect of catechol oestrogen both in terms of stimulation of E and F formation (expressed per mg of tissue) and in its action on product distribution was more marked at lower concentrations of tissue.

17 beta-estradiol and progesterone were administered to post-menopausal women to determine their effects in vivo on the capacity of human endometrium to synthesize prostaglandins (PGs) F2 alpha and E. Basal amounts of PGF2 alpha and PGE synthesized by endometrium exposed to 17 beta-estradiol and progesterone were significantly higher than the levels produced by endometrium exposed to 17 beta-estradiol alone (p less than 0.02 for both PGs). Levels found in the former endometrium were broadly comparable to levels in secretory endometrium and in the latter to amounts found in proliferative endometrium of spontaneous, ovulatory cycles.

Endometrium collected from 18 normal women at various stages of the menstrual cycle was maintained in organ culture for periods of 6 days. Both prostaglandin F2 alpha (PGF2 alpha) and PGE were detected in medium from late proliferative (days 10-14; n = 13) and late secretory (days 20-26; n = 5) endometria cultured in the absence of exogenous steroids. During the first 48 h in culture, the output of PGF2 alpha by secretory endometrium was significantly greater than that of proliferative tissue. The addition of 17 beta-estradiol to the culture medium at doses ranging from 1.0-100.0 ng/ml induced a significant increase in the output of PGF2 alpha by secretory but not proliferative endometria. The addition of progesterone at doses ranging from 5.0-500.0 ng/ml significantly reduced the output of PGF2 alpha and PGE by both proliferative and secretory endometria and prevented the 17 beta-estradiol-stimulated increase in PGF2 alpha output by secretory tissue.