Sertoli cell-only syndrome produced by cold testicular ischemia.
Sertoli cell-only syndrome produced by cold testicular ischemia.
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DOI：
10.1210/endo-122-3-1074
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发表时间：
1988-03
期刊：
影响因子：
4.8
通讯作者：
GEORGE PEI HERNG YOUNG;Marc Goldstein;David M. Phillips;Kalyan Sundaram;G. Gunsalus;C. W. Bardin
中科院分区：
文献类型：
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作者：
GEORGE PEI HERNG YOUNG;Marc Goldstein;David M. Phillips;Kalyan Sundaram;G. Gunsalus;C. W. Bardin
本报告描述了一种新的方法生产支持细胞只有睾丸刘易斯大鼠使用90分钟的低温睾丸缺血。该方法使用手术显微镜辅助下应用的无创伤微夹选择性阻断睾丸血供。在整个缺血期间，将睾丸包裹在冰冷的盐水中，并结扎输精管动脉和静脉。缺血损伤后12周，睾丸重量为对照组睾丸的一半，而前列腺或精囊重量无差异。显微镜检查缺血性损伤的睾丸显示正常外观Leydig和Sertoli细胞，但完全没有生殖细胞。睾丸酶活性测定表明，乳酸脱氢酶和山梨醇脱氢酶减少，而α-谷氨酰转肽酶活性正常，与生殖细胞的显着减少一致。血清雄激素结合蛋白（rABP）水平相对于非缺血对照组升高。相反，血清睾酮、LH和FSH浓度正常。此外，LHRH引起相同的LH和睾酮的反应，在控制和实验动物。用133氙测量的睾丸血流量在仅有支持细胞的睾丸中略有下降。所有组的睾丸内温度均正常。这些观察结果在大鼠缺血诱导的支持细胞只有睾丸是显着不同的辐射或遗传缺陷引起的。患有后一种疾病的动物的FSH水平升高，存在Leydig细胞功能改变的证据，表现为LH升高或对LHRH的异常反应;以及正常或低血清rABP水平。我们的结论是：1）缺血不产生异常的垂体睾丸轴，尽管显着的生殖细胞耗竭和2）支持细胞的睾丸不同病因可以有不同的模式的激素和RABP分泌。
This report describes a new method for producing Sertoli cell-only testes in the Lewis rat using 90 min of hypothermic testicular ischemia. The method employs selective occlusion of the testicular blood supply using atraumatic microclips applied with the aid of an operating microscope. The testis is packed in ice-cold saline throughout the ischemic interval, and the deferential artery and vein are ligated. Twelve weeks after the ischemic insult, the testes weigh half that of control testes while there were no differences in prostate or seminal vesicle weights. Microscopic examination of the ischemic damaged testes revealed normal-appearing Leydig and Sertoli cells, but complete absence of germ cells. Assays of testicular enzyme activities indicated that lactic dehydrogenase and sorbitol dehydrogenase were reduced, while alpha-glutamyl transpeptidase activity was normal, consistent with the marked reduction of germ cells. Serum androgen binding protein (rABP) levels were elevated relative to nonischemic controls. By contrast, serum concentrations of testosterone, LH, and FSH were normal. In addition, LHRH elicited identical LH and testosterone responses in control and experimental animals. Testicular blood flow measured with 133Xenon was slightly decreased in Sertoli-cell-only testes. Intratesticular temperatures was normal in all groups. These observations in rats with ischemia-induced Sertoli-cell-only testes are strikingly different from those induced by radiation or genetic defects. Animals with these latter disorders have elevated FSH levels, evidence of altered Leydig cell function as evidenced by elevated LH or abnormal response to LHRH; and normal or low serum rABP levels. We conclude that 1) ischemia produces no abnormalities of the pituitary testicular axis in spite of marked germ cell depletion and 2) Sertoli-cell-only testes of different etiologies can have varied patterns of hormone and rABP secretion.