Testicular microvascular blood flow is known to exhibit vasomotion, which has been shown to be significantly altered in the short term following the repair of testicular torsion. This loss of vasomotion may ultimately be responsible for the loss of spermatogenesis observed after testicular torsion in rats. In the present study, testicular vasomotion and interstitial oxygen tensions were simultaneously measured prior to, during, and at various time points after repair of testicular torsion in the rat. Testicular torsion was induced by a 720° rotation of the testis for 1 h. Laser-Doppler flowmetry and an oxygen electrode were used to simultaneously measure vasomotion and interstitial oxygen tensions (PO2), respectively. Pretorsion control testes had a mean blood flow of 16.3 ± 1.3 perfusion units (PU) and displayed vasomotion with a cycle frequency of 12 ± 0.2 cycles per minute and a mean amplitude of 4.2 ± 0.3 PU. Mean testicular interstitial PO2 was 12.5 ± 2.6 mm Hg, which displayed a cyclical variation of 11.9 ± 0.4 cycles per minute with a mean amplitude of 2.8 ± 0.8 mm Hg. During the torsion period, both mean blood flow and interstitial PO2 decreased to approximately zero. Upon detorsion, mean microvascular blood flow and mean interstitial PO2 values returned to values that were not significantly different from pretorsion values within 30 min; however, vasomotion and PO2 cycling did not return, even after 24 h. It was 7 days after the repair of torsion before a regular pattern of vasomotion and PO2 cycling returned. These results demonstrate for the first time a correlation between testicular vasomotion and interstitial PO2 cycling, and this correlation persists after the repair of testicular torsion.
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