Estrogen‐induced tumors: Changes in the vasculature in two strains of rat

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Abstract
The influence of estrogen on the vasculature of the pars distalis has been studied in two strains of rat that differ in estrogen responsiveness. (Fischer 344 rats are highly estrogen‐responsive in comparison to Sprague‐Dawley rats.) Ovariectomized adults were implanted with silastic capsules containing 17 β‐estradiol benzoate. Control and experimental animals were sacrificed 10 and 20 days after implantation of the silastic capsules. Pituitary weights and plasma prolactin were elevated dramatically in estrogen‐treated Fischer rats in comparison to more moderate increases in Sprague‐Dawley rats. Although both strains exhibited the hypertrophy of mammotrophs expected after estrogen stimulation, the vasculature in Fischer rats was dramatically altered from normal. The pars distalis of the 20‐day, estrogen‐treated Fischer rats contained well‐formed arteries. In addition, capillaries frequently were disrupted, contributing to the formation of hemorrhagic lakes unlined by an endothelium. Even in intact capillaries, basal laminae delimiting the pericapillary spaces often were disrupted or absent. Perivascular connective tissue cells were prominent within the perivascular spaces and often contained rumerous, large lysosomal dense bodies as well as clusters of small dumbbell‐shaped bodies. These granule clusters also were apparent adjacent to the perivascular space within parenchymal cells, most frequently within follicular cells. The vasculature of Sprague‐Dawley rats maintained a more normal appearance after estrogen treatment, although perivascular connective tissue cells did appear activated and basal laminae delimiting the pericapillary spaces were disrupted occasionally. However, no capillaries were disrupted, nor were any hemorrhagic lakes evident, and no arteries were present. The results indicate that in some strains of rat, estrogen may influence the integrity of the pars distalis vasculature, including the possibility of stimulating vascular reorganization and arteriogenesis. If stimulation of arteriogenesis decreases normal hypothalamic inhibition of mammotrophs, this could be an important factor underlying the formation of prolactinomas.