An analysis of the relationship between mast cell population and the establishment of uterine sensitivity to decidualization in the rat
Gibbons, Ashton Frank Eleazor
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The action of progesterone and estrogen on uterine mast cells of the ovariectomized rat was studied. A single injection of estradiol-17B (0.25 μg) produced a highly significant (P < O.OO1) reduction in both mesometrial and antimesometrial mast cell populations. The mean ± S.E. number of mesometrial and antimesometrial mast cells in the control animals was 19.2 ± 1.3 and 6.3 ± 0.7 respectively, while in the estrogen treated animals the respective values at 15 hours post treatment were 4.1 ± 0.5 and 2.9 ± 0.4. Estrogen treatment also resulted in considerable degranulation of the mast cells. In comparison, progesterone, when administered as a single injection (5 mg) did not produce a drastic reduction of the mast cells. Fifteen hours after its administration, progesterone had produced only a moderate reduction of the mast cell population; however, the decline was significantly smaller than those values obtained at the same time interval following estrogen treatment. Since it is known that progesterone treatment for at least 48 hours, followed by estrogen constitute the basic hormonal sequence for decidualizationin the rat, experiments were designed to study possible relationship between mast cell population and deciduoma development. Results obtained from these experiments demonstrate quite clearly that maximal decidual response was possible only among animals treated over a 48 hour period with progesterone (5 mg/ 24 hours) followed by a small (0.25 μg) injection of estradiol-17B and then traumatized 15 hours later (at a time when mast cell population was reduced to the lowest level). Thus, the hormonal treatment which resulted in the lowest level of mast cell numbers also permitted the largest deciduoma development. Shelesnyak (1957) proposed that histamine play a vital role in decidualization in the rat. On the other hand, it has been shown that mast cell degranulation with the accompanying loss of metachromasia is related to histamine release (Thon, 1967). In order to evaluate the role of estrogen as opposed to that of histamine in decidualization, animals were treated with estrogen and progesterone in addition to an estrogen antagonist -CN-55,945-27. The data from these experiments indicated only a moderate decidual response among the treated animals. In addition, the mast cell population in the uterine wall of these animals, at the time of traumatization, was considerably reduced and degranulated. Thus, uninterrupted estrogen action seems to be necessary for the establishment of sensitivity for maximal deciduoma development. In another set of investigations, uterine mast cells were depleted by administration of compound 48/80. Animals depleted of their mast cells and then treated with progesterone, estrogen, followed by trauma developed only small to moderate deciduomata. However, when rats were allowed to recover for seven days (at which time over 50% of the mast cells had reappeared) and then given the treatment as the preceding group, massive full length deciduoma were produced. The evidence suggests that maximal uterine sensitivity to decidualization is possible only after adequate hormonal treatment, and only in uteri not depleted of mast cells.
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