Sertoli cell-only syndrome produced by cold testicular ischemia.

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.