Our results suggest that propofol as an anesthetic agent may prevent testicular damage by scavenging reactive oxygen and nitrogen species and inhibiting lipid peroxidation in an animal model of testicular torsion and detorsion.
Propofol may offer advantages by inhibiting lipid peroxidation and inflammatory cytokine production in an animal model of gut ischemia/reperfusion-induced liver injury.
To investigate the effects of phosphodiesterase (PDE) 5 inhibitors, sildenafil citrate and vardenafil HCl, on testicular germ cell apoptosis and also on the expressions of eNOS and iNOS within the bilateral testis after a unilateral torsion in a rat model. Forty-eight Wistar Albino rats, weighing between 210 and 262 g, were housed in individual cages. The rats were randomly assigned into four main groups and each group received drugs. Saline, sildenafil citrate and vardenafil HCl were given to each for 1 month and the last received no drug. After 1 month, testicular torsion was created for 1 h of ischemia and the left testis was untwisted and replaced to the scrotum for 2 h of reperfusion. At the end of 3 h, contralateral and ipsilateral testes were removed for histopathologic and biochemical examinations. Under light microscopy; the histopathological patterns of the contralateral testes in all groups were not affected. Mean apoptotic cell, eNOS and iNOS levels were increased in saline study group. The rats treated with vardenafil and sildenafil (groups 2s and 3s) showed significantly increased apoptotic cell, eNOS and iNOS values in ipsilateral testis (P < 0.05). Sildenafil citrate and vardenafil HCl caused an exaggerated testicular apoptosis after IR injury in rats. Additionally these drugs increased the NOSs levels in the testicular tissue.
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