The effects of chemical sympathectomy on testicular injury in varicocele.

Abstract

To determine whether the sympathetic nervous system plays a role in the contralateral testicular deterioration encountered in varicocele. Forty male Sprague-Dawley albino rats (28 days old) were divided equally into four treatment groups, i.e. (1) sham operation, (2) with varicocele, (3) treated by chemical sympathectomy plus varicocele, and (4) chemical sympathectomy only. Chemical sympathectomy was induced by administering intraperitoneal 6-OH dopamine (100 microg/g for 5 days) in groups 3 and 4; groups 1 and 2 received equal volumes of physiological saline by the same route. All rats underwent laparotomy and part of the left renal vein (distal to the spermatic vein confluence) was isolated and encircled with a 4/0 silk suture. The suture was left untied in group 2, and tied around a 24 F peripheral venous cannula in groups 3 and 4. The testes were then excised when the rats were 70 days old; malondialdehyde (MDA) in the testicular tissue was assayed by the thiobarbituric acid-reactive substances method, and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels were determined by spectrophotometric analysis. Varicocele resulted in a significant increase in MDA levels in both testes and chemical sympathectomy prevented this effect. SOD and GSH-Px values were significantly decreased in both testes in group 2; chemical sympathectomy also prevented this effect. An induced unilateral varicocele significantly increases the biochemical indicators of tissue hypoxia in both testes. As this increase was prevented by chemical sympathectomy, the sympathetic nervous system may play a role in the testicular degeneration associated with varicocele.