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Effect of replication-defective herpes simplex virus mediated kynurenine aminotransferase on detrusor overactivity in rats with spinal cord injury / 中华泌尿外科杂志
Chinese Journal of Urology ; (12): 108-112, 2015.
Artículo en Chino | WPRIM | ID: wpr-470680
ABSTRACT
Objective To evaluate if replication-defective herpes simplex virus mediated kynurenine aminotransferase Ⅱ (HSV-KAT Ⅱ) could inhibit detrusor overactivity (DO) in rats with spinal cord injury by bladder wall injection.Methods From June 2012 to July 2013,48 male Wistar rats with T10 spinal cord transection (SCT) were randomly divided into normal saline group,HSV group and HSV-KAT Ⅱ group (n=16 each group).Normal saline (40 μl),HSV or HSV-KAT Ⅱ (40 μl,1×107 plaque forming unit viruses) was injected into the rat bladder wall of according group by 1 week after SCT.Three weeks after injection,cystometry was performed and the virus transfected efficiency,expression of KAT Ⅱ in L6-S1 dorsal root ganglia were examined.Results The DO number,DO amplitude,maximum voiding pressure and volume inducing voiding were decreased significantly by 59.6%-61.1%,21.6%-24.2%,30.3%-34.4% and 44.1%-46.5% (P<0.01),while voiding efficiency,the time to first DO were increased significantly by 40.7%-47.7% and 30.1%-49.0% (P<0.01) in the HSV-KAT Ⅱ group compared with normal saline group and HSV group.However,the leaking volumes were no significantly different among the 3 groups (P>0.05).The relative intensity of KAT Ⅱ protein (0.50±0.13 versus 0.28±0.07,P<0.05) and mRNA (0.78±0.06 versus 0.51±0.08,P<0.01) were increased significantly in HSV-KAT Ⅱ group than those in HSV group.Conclusion HSV-KATⅡ bladder wall injection inhibits DO and may improve detrusor-sphincter dyssynergia in rats with spinal cord injury.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Urology Año: 2015 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Urology Año: 2015 Tipo del documento: Artículo