Azoospermia and maturation arrest: malfunction of valves in erect poster of humans leads to hypoxia in sperm production site

Abstract

Maturation arrest (MA) of spermatogenesis is diagnosed on histology as interruption of spermatogenesis before the final stage without impairment of Sertoli or Leydig cells. It is considered a condition of irreversible or absolute infertility. Varicocele, which represents impairment in the testicular venous drainage system, has been shown to be a bilateral disease. Malfunction of the valves increase the hydrostatic pressure in the testicular venous system that exceeds the pressure in the arterial system leading to hypoxia in the testicular microcirculation and in the seminiferous tubules, the sperm production site. Sperm production deteriorates, and ultimately progresses to azoospermia. Our prediction was that MA, if genetic factors are excluded, is the final stage of long standing hypoxia. This would indicate that MA is not always an independent disease entity, but may represent progressive process of deterioration of the testicular parenchyma beyond azoospermia. By histology and electron microscopy, our prediction confirmed, at least partially, that MA is associated with degenerative ischaemic changes in the seminiferous tubules. Adequate treatment of bilateral varicocele by microsurgery or super-selective sclerotherapy of the internal spermatic veins including associated network of venous bypasses, vertically oriented, may resume the flow of oxygenated blood. If irreversible damages did not occur and ischaemia is not too long standing, limited sperm production may be restored, at least partially.

Expression of estrogen receptors-α in testicular biopsies from nonobstructive azoospermic patients

“…These results were in agreement with those of previous investigators who have reported findings similar to those of our study [21,22]. There was arrest of maturation at primary spermatocytes and marked cytoplasmic vacuolation of some germ cells.…”

Hydrodynamic Relationship between Color Doppler Ultrasonography Findings and the Number of Internal Spermatic Veins in Varicoceles

“…This higher static pressure is similar with traffic jams in a bottleneck. Although Gat, et al6,7,21-24 suggested that hydrostatic pressure depends only on the vertical height of the ISVs, we conjecture that hydrostatic pressure depends on not only the vertical height of the ISVs but also the division of the ISVs. Also, we feel that this static pressure, due to the division of the ISVs, might also have some influence on the affected testis.…”

“…Varicocele is caused by increased hydrostatic pressure in the impaired testicular venous drainage system 6,7,21-24. Gat, et al6,7,21-24 found that due to the destruction of one-way valves, pathologic hydrostatic pressure is produced in the testicular venous microcirculatory system about 5 times higher than normal, exceeding arteriolar pressure. The pressure gradient between the arterioles and venules in testicular tissue is thereby reversed, leading to persistent hypoxia in the seminiferous tubules, as well as in Sertoli and Leydig cells.…”

“…The pressure gradient between the arterioles and venules in testicular tissue is thereby reversed, leading to persistent hypoxia in the seminiferous tubules, as well as in Sertoli and Leydig cells. Hypoxia due to varicocele may cause progressive deterioration of sperm production, and may further lead to azoospermia and then finally to maturation arrest 7,22,24…”

Reversible Effect of High Altitude on Rat Testis Morphology and Spermatogenesis: Histological and Ultrastructural Study

“…This is because the partial pressure of oxygen decreases and the amount of oxygen available for diffusion into blood stream also decreases (Beall et al, 1994). High altitude hypoxia (hypobaric hypoxia, HH) is said to reduces fertility in humans (Farias et al, 2005a;Cikutovic et al, 2009;Hwang et al, 2009;Gat et al, 2010aGat et al, , 2010b. However, epidemiological studies of high and low altitude populations did not support this hypothesis (Vitzthum & Wiley, 2003;Bartsch et al, 2004).…”