This study reports on the stagnation of blood within the microcirculatory vessels of the testes of patients with varicocele. Both fine structural and quantitative studies were carried out on testicular biopsies from 14 men with varicocele and a control group of three men. Arterioles, capillaries, and venules were completely filled with blood in all affected testes. Enlarged pores were also noticed between the endothelial cells of these affected vessels. Lumen diameters of the arterioles were significantly decreased in the affected testis compared to controls. No change in the overall diameter of the arterioles and venules was noted. Significant thickening of the limiting membrane was also noted in the affected testis. It was concluded that the stagnation of blood in the microcirculatory vessels may cause local hypoxia and ischemia, which lead to spermatogenic disorders.

A systematic investigation of the effects of unilateral torsion of the spermatic cord on the contralateral testis of the guinea pig was carried out for variable time periods, ie, seven days, one, three and six months. Both histological and ultrastructural studies were made on all testicular autopsy materials collected from five groups of animals. Those five groups were: group I, 12 animals with unilateral torsion induced and maintained until the day of sacrifice; group II, 12 animals with unilateral torsion induced for four hours; group III, eight sham‐operated animals; group IV, eight pentobarbital injected animals; group V. four untreated control animals. Of 24 group I and group II animals, degenerative changes were noticed in the contralateral testis in ten animals. Those changes ranged from spermatid and spermatocyte degeneration to the complete loss of all types of germ cells in the contralateral testis. The degree of damage seemed to correlate with the severity of damage in the torsion‐side testis and the length of time the damaged testis was retained in the body. It was concluded that a damaged testis retained in the body may cause degenerative changes in the contralateral testis.

No abstract

The fine structure of the contralateral, so-called unaffected, testis of two of three patients with unilateral testicular torsion revealed varying degrees of abnormalities, apparently related to the time course of the condition. In one patient (H-87) with unilateral torsion of 16 days duration, the contralateral testis revealed various morphological abnormalities. These included abnormal nuclear condensation in spermatids, disappearance of the inner component of the basal lamina, degeneration of the germinal epithelium, and "intermixing" of germinal epithelial cells with peritubular components. In the other patient (H-109) with severe atrophy of one testis as a result of torsion, the contralateral testis revealed abnormalities which included spermatids with degenerating heads and tails within the Sertoli cell cytoplasm near the basal lamina and peritubular thickening accompanied by a greater than usual number of Leydig cells. In guinea pigs with experimentally induced unilateral torsion, abnormal spermatid development was seen in the contralateral testis of those animals in which the affected testis was severely damaged. Moreover, the Sertoli cells exhibited a high degree of phagocytic activity. Fewer abnormal spermatids in the spermatogonial compartment were found in the contralateral testis of the animals which had only moderately altered histology of the affected testis. No fine structural change was noted in the contralateral testis of control or sham operated animals or in those which displayed only minimal damage in the affected testis. This study suggests that unilateral torsion of the spermatic cord resulting in moderate to severe damage to the affected testis may be associated with morphological abnormalities in the contralateral testis.

Bilateral testicular biopsies from four men with a short duration (3 hours 10 minutes to 4 hours 30 minutes) of unilateral spermatic cord torsion and testicular biopsies from six men with irreversible brain death were used for the present investigation. Extensive light and electron microscopic studies and quantitative analyses of all biopsy materials were performed. The torsioned testes revealed variable degrees of damage to the seminiferous tubules, including germ cell disorganization and sloughing of immature germ cells. Ninety‐five percent of the blood vessels from the biopsied tissue specimens were clogged with blood cells. The seminiferous tubules of the contralateral testis had normal germ cell arrangements and counts. However, 88% of the microvessels from the tissue biopsied from the contralateral testes were packed with blood cells, whereas only 10% of the blood vessels in the control biopsy specimen were clogged with blood cells. At the electron microscopic level, fewer tight junctions and enlarged pores were found between the endothelial cells of the affected vessels, and microvilli were completely absent from these endothelial cells. The clogging caused by blood cells in the affected vessels was so severe that no space was found between the membrane of the endothelial cell and the membrane of the blood cells. It has been suggested that local clogging by blood is responsible for the initiation of degenerative changes in the testes of men with unilateral torsion of the spermatic cord.