Katovich M J, Cameron D F, Murray F T, Gunsalus G L
J Androl. 1985 May-Jun;6(3):179-89. doi: 10.1002/j.1939-4640.1985.tb00834.x.
The effects of hyperprolactinemia on testicular structure and pituitary-gonadal function were investigated in male rats. Hyperprolactinemia was induced in the Wistar-Furth rat by implantation of tissue fragments of a prolactin-secreting MtTW15 pituitary adenoma. The MtTW15 tissue was maintained in one animal group for 27 days (group A) and in another group for 37 days (group B). Appropriate age-matched controls were utilized in each study. Serum prolactin was significantly elevated (P less than 0.001) in both groups of MtTW15-bearing rats compared with their controls. The degree of hyperprolactinemia was more severe in rats of group B (2842 +/- 546 ng/ml) than in rats of group A (367 +/- 38 ng/ml). Accessory sex organ weights in group B rats were significantly lower than in controls, but were apparently unaffected in group A rats. Hyperprolactinemia induced definite but variable testicular alterations in both animal groups that presented as seminiferous epithelial disorganization, germ cell exfoliation, increased tubule wall thickness, and abnormal Leydig cell lipid content. Electron microscopy revealed structural disruption of Sertoli-germ cell junctional complexes and apical Sertoli cell cytoplasmic degeneration. The hyperprolactinemic rat exhibited significant reductions in serum luteinizing hormone (LH), testosterone (T), and androgen binding protein (ABP) when compared with controls. Eighty-six days following surgical removal of the MtTW15 tissue in a subgroup of group B rats, serum levels of prolactin and LH returned to normal, as did weights of accessory sex organs and testicular morphology. These results indicate that exposure to the MtTW15 adenoma and its later removal in the rat provides a workable model for studying the effects of hyperprolactinemia on testicular structure and function, and for identifying events involved in the subsequent recovery of spermatogenic disruption.
在雄性大鼠中研究了高催乳素血症对睾丸结构和垂体-性腺功能的影响。通过植入分泌催乳素的MtTW15垂体腺瘤组织碎片，在Wistar-Furth大鼠中诱导高催乳素血症。将MtTW15组织在一组动物中维持27天（A组），在另一组中维持37天（B组）。每项研究都使用了年龄匹配的适当对照。与对照组相比，两组携带MtTW15的大鼠血清催乳素均显著升高（P<0.001）。B组大鼠（2842±546 ng/ml）的高催乳素血症程度比A组大鼠（367±38 ng/ml）更严重。B组大鼠的附属性器官重量显著低于对照组，但A组大鼠的附属性器官重量显然未受影响。高催乳素血症在两个动物组中均引起了明确但可变的睾丸改变，表现为生精上皮紊乱、生殖细胞脱落、小管壁厚度增加以及睾丸间质细胞脂质含量异常。电子显微镜显示支持细胞-生殖细胞连接复合体的结构破坏和支持细胞顶端细胞质变性。与对照组相比，高催乳素血症大鼠的血清促黄体生成素（LH）、睾酮（T）和雄激素结合蛋白（ABP）显著降低。在B组大鼠的一个亚组中，手术切除MtTW15组织86天后，血清催乳素和LH水平恢复正常，附属性器官重量和睾丸形态也恢复正常。这些结果表明，在大鼠中暴露于MtTW15腺瘤及其随后的切除为研究高催乳素血症对睾丸结构和功能的影响以及确定生精破坏后续恢复过程中涉及的事件提供了一个可行的模型。
