Rescue of testicular function after acute experimental torsion

Spermatic cord torsion results in impairment of testicular function. The mechanism of this injury is unclear; however, intracellular Ca++ influx and reactive oxygen species have been implicated in the testicular damage following torsion and reperfusion. In the present study a model of testicular torsion in the rat was used to determine whether testicular function following torsion can be rescued by the administration of antioxidants and Ca++ channel blockers.

Seventy-two animals were divided into 9 groups. Animals underwent 1 hr. or 2 hrs., 720 degrees experimental torsion. Animals received combinations of superoxide dismutase (SOD), catalase, allopurinol, and verapamil. Drugs were administered intravenously during the last 15 minutes of experimental torsion and the first hour of reperfusion. Bilateral testicular function was determined 60 days after experimental torsion by measuring testis weights, daily sperm production (DSP), and testicular venous testosterone concentrations. Ipsilateral values were compared to both control and contralateral values.

SOD + catalase and SOD + catalase+verapamil treatments caused significant rescue of tests function following 1 hr. experimental torsion. Mean +/- s.e. testis weights and DSP in control animals were 1.75 +/- 0.6 g. and 18.4 +/- 0.3 x 10(6) sperm/g./d. The same value for testes experiencing 1 hr. experimental torsion were 0.72 +/- 0.6 g. and 2.3 +/- 0.5 x 10(6) sperm/g./d. The values from testes receiving 1 hr. experimental torsion followed by SOD + catalase were 1.45 +/- 0.17 g. and 9.9 +/- 1.8 x 10(6) sperm/g./d. Neither allopurinol nor verapamil added benefit. No significant rescue was seen in testes undergoing 2 hrs. experimental torsion.

Treatment with oxygen radical scavengers provides significant rescue of testicular function after acute experimental torsion.