Cellular responses to experimental inhibition of collagen degradation in the postpartum rat uterus

Abstract

AbstractRapid collagen breakdown in the postpartum rat uterus is accompanied by rising collagenase activity (Jeffrey and Gross, '70) and a transient infiltration of the stroma by heterophils, eosinophils, monocyte‐macro‐phages, lymphocytes, and plasma cells (Padykula and Campbell, '76), cells usually associated with inflammatory response. This uterine catabolism is initiated soon after birth while blood estrogen and progesterone levels are low. To investigate the hormonal factors involved in regulation of this postpartum stromal differentiation, we analyzed the cytological effects of experimentally elevating progesterone and estradiol levels in the peripartum period by following the protocol of biochemical experiments that have demonstrated inhibition of collagenase activity by progesterone (Koob and Jeffrey, '74) and estradiol (Ryan and Woessner, '74).Prolonged gestation (progesterone, 10 mg/day starting on day 19 gestation) was used as a condition to prevent the prenatal drop in blood progesterone; this treatment was the most effective in blocking postpartum stromal differentiation. It preserved the state of prepartum uterine differentiation and most importantly it prevented monocytic‐macrophagic conversion. Progesterone (40 mg/day) given at birth delayed but did not block stromal differentiation during the first 48 hours; by 72 hours collagen loss was extensive in both control and progesterone‐treated rats and numerous macrophages were present. Estradiol (100 μg/day) given at birth caused a greater delay in stromal differentiation than progesterone given at birth; for approximately 48 hours the number of eo‐sinophils, heterophils, and macrophages was less than normal. By day 3 the number and distribution of the macrophages resembled that of the day 1 control uteri. Overall these experiments indicate that the low estrogen and progesterone levels at birth are essential for normal stromal regression. Since these transient cells originate from the blood, the temporal pattern of their emigration into the uterus may be under hormonal control. Experimental disturbance of this pattern influences the course of collagen resorption.