Corrales J J, Kadohama N, Chai L S, Hoisaeter P A, Hampton M T, Murphy G P, Sandberg A A
Prostate. 1981;2(4):337-58. doi: 10.1002/pros.2990020403.
The mechanism by which estrogens inhibit castration atrophy has been investigated morphologically and biochemically utilizing ventral prostate from Copenhagen rats. The suppression of weight loss and gross edematous appearance of the prostate associated with the in vivo effect of 17 beta-estradiol (E2) could not be accounted for by DNA and protein synthesis. Increase in the fluid content in the tissues was confirmed by demonstration of significant increase in the ratio of wet/dry tissue weights. Light microscopy demonstrated that the main effects were on the stroma, characterized by large interglandular areas almost totally devoid of collagen resulting in an edematous appearance. Electron microscope studies showed an abundance of fluid localized adjacent to the capillary endothelium and some red blood cells indicating disturbances in capillary permeability. The combination of a prolactin secretion inhibiting agent with E2 alone, indicating an involvement of prolactin the estrogen effect. Differences in blood prolactin concentration between the strains of rats may influence the sensitivity of the prostate to estrogens.
利用哥本哈根大鼠的腹侧前列腺，从形态学和生物化学方面研究了雌激素抑制去势萎缩的机制。与17β-雌二醇（E2）的体内作用相关的前列腺重量减轻和明显水肿外观的抑制，无法用DNA和蛋白质合成来解释。通过显示湿/干组织重量比显著增加，证实了组织中液体含量的增加。光学显微镜显示主要作用于基质，其特征是腺间区域大，几乎完全没有胶原蛋白，导致水肿外观。电子显微镜研究显示，大量液体位于毛细血管内皮附近，还有一些红细胞，表明毛细血管通透性受到干扰。催乳素分泌抑制剂与单独使用E2的联合作用，表明催乳素参与了雌激素效应。大鼠品系之间血液催乳素浓度的差异可能会影响前列腺对雌激素的敏感性。
