To study the mechanism for the adaptive mucosal hyperplasia which occurs independent of luminal nutrition and pancreatico-biliary secretions in isolated Thiry-Vella segments of intestine from lactating rats, and to examine the effects of prolactin on small bowel mucosal structure in the rat, we used two models of experimental hyperprolactinaemia and compared quantitative histology and several markers of mucosal mass in jejunum and ileum from control rats and from test and lactating animals. Hyperprolactinaemia, induced by perphenazine injections (5 mg/kg/day for two or seven weeks) or transplantation of four pituitary glands from donor animals to beneath the renal capsule in the recipient, was confirmed by radioimmunoassay. Proof of its biological activity was obtained by weighing the mammary pads and by demonstrating true breast hyperplasia on histological section. Median serum prolactin levels increased from 50 ng/ml in the controls to 570 ng/ml in the perphenazine treated animals and to 600 ng/ml in the pituitary transplanted rats-levels comparable with those seen in lactation (870 ng/ml). In the lactating rats, there was striking mucosal hyperplasia of both jejunum and ileum but, despite the hyperprolactinaemia, there were no such changes in villus height, crypt depth, or in mucosal wet weight, protein, or DNA/unit length intestine in the perphenazine-injected or pituitary-transplanted animals. We conclude that prolactin is not atrophic to the intestine in rats and that hyperprolactinaemia cannot explain the intestinal adaptive changes of lactation.
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