SUMMARY
A single injection of oestradiol given to ovariectomized mice pretreated with progesterone for several days stimulates a large increase in cell division in the uterine stroma which reaches a maximum 24 hr. later. A second injection 48 hr. after the first, also stimulates stromal cell division, but a second injection 12–36 hr. after the first does not. This failure to respond is not due simply to depletion of the stock of cells ripe for division. Rather it appears that the uterus becomes insensitive to further stimulation for approximately 36 hr. Although a second injection 24 hr. after the first injection does not increase stromal cell division, it does lengthen the refractory period so that a third injection given at 48 hr. has no effect.
Metritis is an important disorder in dairy cows during the early postpartum period. Myometrial contractility is a prerequisite for uterine involution; however, very scanty literature is available about the effect of metritis on this process and endocrine responsiveness. This study was aimed to evaluate the effect of inflammation on uterine contractility in vitro, and the inflammation was induced by incubating myometrial strips with lipopolysaccharides (LPS). Myometrial samples were collected from 17 healthy Holstein Friesian cows during caesarean section. Eight longitudinal strips from each cow were incubated in organ baths with LPS concentrations of 0 (LPS0), 0.1 (LPS0.1), 1 (LPS1) and 10 µg/ml (LPS10). Spontaneous contractility and contractility induced by increasing concentrations of oxytocin (10–10 – 10–7 mol/L) were recorded during nine 30‐min intervals (T1 to T9). The minimum amplitude (minA), maximum amplitude (maxA), mean amplitude (meanA) and area under the curve (AUC) were calculated for each time interval. LPS had an effect (p ≤ .05) on maxA, meanA and AUC. In T1, myometrial strips incubated with LPS0.1 and LPS1 had higher (p ≤ .05) maxA, meanA and AUC than the strips incubated with LPS0. In T9 without oxytocin, LPS0 led to higher (p ≤ .05) maxA, meanA and AUC than LPS0.1 and LPS1. In T8 and T9 with oxytocin, LPS1 had lower (p ≤ .05) maxA, meanA and AUC than the other LPS concentrations. Interestingly, the results show that LPS has a transient positive effect on myometrial contractility in vitro and that this effect is dependent on LPS concentration and duration of incubation.
The non-steroidal antioestrogen tamoxifen (trans-1-(4-beta-dimethylaminoethoxyphenyl)-1,2-diphenylbut- 1-ene), widely used in the treatment of breast cancer, and its oestrogenic cis-isomer rapidly inhibited contractile responses of isolated rat myometrium to supramaximal concentrations of oxytocin (1.28 X 10(-6) mol/l). Both compounds were effective at concentrations comparable with the plasma concentrations of tamoxifen reached in therapy (i.e. 5 X 10(-7) to 5 X 10(-6) mol/l). Inhibition was too rapid in onset (less than 3 min) to involve changes in RNA transcription and protein synthesis, and was not prevented or reversed by the addition of oestradiol to the bath. We conclude that the inhibition did not involve the classical oestrogen receptor pathway. Oestradiol-17 beta at concentrations above 10(-6) mol/l also inhibited the myometrium and potentiated the effects of the anti-oestrogens. Our experiments suggest that the anti-oestrogens and oestradiol act via a similar route with tamoxifen having an equilibrium affinity approximately tenfold greater than that of oestradiol.
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