Male infertility

The prevalence of male infertility in the general population is 5%. Among persons with varicocele, however, 1941% (33% is a generally accepted figure) suffer from primary infertility. Typically, these patients' seeded player samples show diminished sperm counts, decreased motility, and immature cellular morphology.

The precise pathophysiologic mechanisms responsible for such phenomenon currently remain unappreciated (3:861). Various hypotheses for the alteration of spermatogenesis swallow included the following: ebbing of toxic metabolites from either adrenal or renal origins; excited hormone status; spermatic venous hypertension; testicular hypoxia secondary to stasis; and abnormal temperature

order (2:149). Various investigations have examined the possibility that toxic metabolic byproducts--such as prostaglandins--may reach the testicles through changes in venous circulation.

In addition, researchers have postulated that infertility could result from alteration of the hypothalamicpituitarygonadal hormone axis. A third pathophysiologic mechanism might take in the "nutcracker phenomen." This could occur upon coalescency of the left renal venous blood vessel between the abdominal aorta and the superior mesenteric artery. Such compression may cause spermatic venous hypertension. Additionally, a simplification in the rate of blood flow through the pampiniform plexus might result in decreased oxygen availability. Lastly, it has been spy that a left varicocele raises
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