Unremitting Suppression of the Postovariectomy Rise in Plasma LH by Tumor-Induced Hyperprolactinemia

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Abstract
The plasma LH response to ovariectomy was studied at different periods in the development of hyperprolactinemia in rats bearing the transplantable prolactin-secreting pituitary tumors 7315a or MtTW15. Rats were subcutaneously inoculated with tumor cells and ovariectomy was performed at 3 times during the subsequent growth of the solid tumor: (1) coincident with tumor cell implantation; (2) when solid tumors first became palpable, and (3) when solid tumors were large. The values for circulating prolactin and LH were serially determined following ovariectomy for 63, 35 and 28 days, respectively. In other studies, tumor cells were implanted into animals which had undergone ovariectomy 3 months earlier. In the presence of hyperprolactinemia caused by the prolactin secreting tumors, the plasma LH following ovariectomy was either reduced following an initial increase, prevented from increasing, or reduced from chronically elevated levels. Hyperprolactinemia of approximately 7–50 μg/ml caused marked suppression of LH secretion, while hyperprolactinemia in the range of 0.2–6 μg/ml resulted in significant but slower and lesser suppression of LH which did not reach noncastrate levels. The inhibitory effect of hyperprolactinemia on plasma LH after ovariectomy was persistent and unremitting for the duration of each experiment, and there was no tendency for suppressed LH to return to levels expected for the ovariectomized state. The model of hyperprolactinemia induced with transplantable prolactin-secreting tumors in the ovariectomized rat may prove to be valuable in understanding the mechanism of depression of gonadal function by hyperprolactinemia.