Daehlin L
Scand J Urol Nephrol Suppl. 1985;91:1-44.
In vitro incubations of human testicular tissue responded to human chorionic gonadotrophin with testosterone release in a dose-dependent manner. The release of testosterone increased with incubation time. The stimulated release of testosterone was inhibited by oestradiol and ethinyl oestradiol in a dose-dependent manner, suggesting that these oestrogens exert direct inhibitory effects on the human Leydig cells. Estramustine phosphate, estromustine, diethylstilboestrol and diethylstilboestrol diphosphate did not inhibit testosterone release. Hypophysectomized rats were treated for 8-9 days with human chorionic gonadotrophin, which maintained testicular blood flow within the physiological range. Some of the animals received additional treatment with oestradiol or estromustine. Oestradiol and estromustine depressed plasma testosterone concentration. In contrast to estromustine, oestradiol inhibited testicular blood flow, as measured by the microsphere technique. Intact rats were castrated, supplemented with testosterone and concomitantly treated with different oestrogenic substances. Testosterone supplementation induced increase of prostatic blood flow, which was inhibited by oestradiol, ethinyl oestradiol or diethylstilboestrol. Estramustine and estromustine had no effect on prostatic blood flow. The growth of a transplantable rat prostatic carcinoma (Dunning R3327H) was studied after castration, testosterone substitution or testosterone substitution in combination with oestradiol treatment. Oestradiol inhibited tumour growth, possibly by direct action. The blood flow in tumours in intact animals decreased with increasing tumour volume. Oestradiol treatment enhanced tumour blood flow. The oestrogenic effects of estramustine phosphate, ethinyl oestradiol/polyoestradiol phosphate or orchiectomy were studied in previously untreated prostatic carcinoma patients by measuring serum levels of liver proteins (pregnancy zone protein and sex hormone binding globulin) and pituitary hormones (luteinizing hormone, follicle stimulating hormone and prolactin) during a 6 month period. Both medical treatments induced marked but quite comparable changes of the proteins. Apart from the increase of follicle stimulating and luteinizing hormones, no changes were observed in these serum proteins after orchiectomy.
人睾丸组织的体外孵育对人绒毛膜促性腺激素有反应,睾酮释放呈剂量依赖性。睾酮释放量随孵育时间增加。雌二醇和炔雌醇以剂量依赖性方式抑制睾酮的刺激释放,表明这些雌激素对人睾丸间质细胞有直接抑制作用。磷酸雌莫司汀、雌莫司汀、己烯雌酚和己烯雌酚二磷酸酯不抑制睾酮释放。对垂体切除的大鼠用人绒毛膜促性腺激素治疗8 - 9天,可使睾丸血流维持在生理范围内。部分动物额外接受雌二醇或雌莫司汀治疗。雌二醇和雌莫司汀降低血浆睾酮浓度。与雌莫司汀不同,用微球技术测量显示,雌二醇抑制睾丸血流。对完整大鼠进行去势、补充睾酮并同时用不同雌激素物质治疗。补充睾酮可使前列腺血流增加,这被雌二醇、炔雌醇或己烯雌酚抑制。雌莫司汀和雌莫司汀对前列腺血流无影响。研究了去势、睾酮替代或睾酮替代联合雌二醇治疗后可移植大鼠前列腺癌(邓宁R3327H)的生长情况。雌二醇可能通过直接作用抑制肿瘤生长。完整动物肿瘤中的血流随肿瘤体积增大而减少。雌二醇治疗可增加肿瘤血流。通过在6个月期间测量前列腺癌患者血清中肝蛋白(妊娠区蛋白和性激素结合球蛋白)和垂体激素(促黄体生成素、促卵泡生成素和催乳素)水平,研究了磷酸雌莫司汀、炔雌醇/聚磷酸雌二醇或去势对未经治疗的前列腺癌患者的雌激素作用。两种药物治疗均引起这些蛋白显著但相当的变化。除促卵泡生成素和促黄体生成素增加外,去势后这些血清蛋白未观察到变化。