Abstract
Testis blood flow per testis closely follows testis weight in rats made aspermatogenic by a single exposure of the testis to 43 degrees C for 30 min or 500 rad (5 Gy) of irradiation from a caesium source, or following ligation of the efferent ducts. Aspermatogenesis following these treatments was associated with only minor changes in the concentrations of testosterone in peripheral blood before stimulation with human chorionic gonadotrophin (hCG), and a reduced responsiveness to hCG when testis weight had fallen after heating. The concentrations of testosterone in testicular venous blood was normal or above normal during aspermatogenesis resulting from heat or irradiation, and only slightly reduced following efferent duct ligation. Consequently testosterone production (defined as the product of plasma flow and the veno-arterial concentration difference for testosterone) was markedly reduced during aspermatogenesis, both before and after stimulation with hCG. It appears that the reduced blood flow limits the amount of testosterone leaving the testis, and while the Leydig cells are capable under some circumstances of compensating partially for this fall by increasing the concentration of testosterone in the testicular venous blood, this compensation is not complete when there are severe reductions in blood flow. Therefore one can conclude that the mass of the tubules is the main determinant of testis blood flow and the Leydig cells must manage with what the tubules require.
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