Urakami Shinji, Shiina Hiroaki, Enokida Hideki, Kawamoto Ken, Kikuno Nobuyuki, Fandel Thomas, Vejdani Kaveh, Nunes Lora, Igawa Mikio, Tanagho Emil A, Dahiya Rajvir
Department of Urology, Veterans Affairs Medical Center, University of California, 4150 Clement Street, San Francisco, CA 94121, USA.
World J Urol. 2007 Apr;25(2):207-13. doi: 10.1007/s00345-006-0142-7. Epub 2007 Jan 13.
Spinal cord injury (SCI) rostral to the lumbosacral level causes bladder hyperreflexia and detrusor-sphincter dyssynergia (DSD), which are accompanied by bladder hypertrophy. We hypothesize that bladder augmentation using a bladder acellular matrix graft (BAMG) can improve the function of SCI-mediated neurogenic bladder. In female rats (n = 35), SCI was induced by transection of the spinal cord at the lower thoracic level. Eight weeks following spinalization, bladder augmentation using BAMG was performed after hemicystectomy of the hypertrophic bladder. Cystometrography was performed at 8 weeks after spinalization and again at 8 weeks after augmentation. Several urodynamic parameters were measured and the grafted bladder was histologically evaluated. Thirty one rats were alive 8 weeks after spinalization. Twenty two (71%) rats developed hyperreflexic bladders and nine (29%) rats had underactive bladders before bladder augmentation. Twenty six rats survived until 8 weeks after augmentation. Urodynamic parameters showed improvement in some bladder functions in both hyperreflexic and underactive bladders after augmentation. In addition, bladder compliance was increased in hyperreflexic bladders and decreased in underactive bladders. Bladder augmentation decreased bladder capacity in high-capacity rats and increased it in low-capacity rats. Histological evaluation showed complete regeneration of BAMG in SCI-induced neurogenic bladder at 8 weeks after augmentation. This is the first report suggesting that the voiding function in SCI-induced neurogenic bladder can be improved by augmentation using BAMG. Improved voiding function was accompanied by histological regeneration of BAMG.
腰骶水平以上的脊髓损伤会导致膀胱反射亢进和逼尿肌-括约肌协同失调(DSD),并伴有膀胱肥大。我们假设使用膀胱脱细胞基质移植物(BAMG)进行膀胱扩大术可以改善脊髓损伤介导的神经源性膀胱的功能。在雌性大鼠(n = 35)中,通过在胸段下部横断脊髓诱导脊髓损伤。脊髓损伤8周后,在对肥大膀胱进行半膀胱切除术后,使用BAMG进行膀胱扩大术。在脊髓损伤后8周和扩大术后8周分别进行膀胱压力容积测定。测量了几个尿动力学参数,并对移植膀胱进行了组织学评估。脊髓损伤8周后,31只大鼠存活。在膀胱扩大术前,22只(71%)大鼠出现膀胱反射亢进,9只(29%)大鼠膀胱活动低下。26只大鼠存活至扩大术后8周。尿动力学参数显示,扩大术后,膀胱反射亢进和膀胱活动低下的膀胱的某些功能均有改善。此外,膀胱反射亢进的膀胱顺应性增加,膀胱活动低下的膀胱顺应性降低。膀胱扩大术使高容量大鼠的膀胱容量减小,低容量大鼠的膀胱容量增加。组织学评估显示,扩大术后8周,BAMG在脊髓损伤诱导的神经源性膀胱中完全再生。这是第一份表明使用BAMG进行扩大术可改善脊髓损伤诱导的神经源性膀胱排尿功能的报告。排尿功能的改善伴随着BAMG的组织学再生。