Guven Ahmet, Kalorin Carmin, Onal Bulent, Whitbeck Catherine, Chichester Paul, Kogan Barry A, Levin Robert M, Mannikarottu Anita
Section of Pediatric Urology, Albany Medical College, Albany, New York, USA.
Neurourol Urodyn. 2007;26(7):1036-42. doi: 10.1002/nau.20433.
Partial bladder outlet obstruction (PBOO) results in marked contractile, biochemical, and histological alterations in the bladder. Our aim was to determine the time course of progressive PBOO in the rabbit and to find parameters that marked the shift to decompensation.
Twenty-four rabbits were subjected to 1, 2, 4, and 8 weeks of PBOO. Sham operated rabbits served as controls. At each time period, cystometry was performed and individual bladder strips were used for contractility studies. Full-thickness sections of bladder body from each rabbit were fixed in formalin and used to determine the vascular density and nerve density. The balance of the bladder body was separated between muscle and mucosa and was analyzed for superoxide dismutase (SOD) and catalase (CAT) activities.
Bladder weight increased progressively and all contractile responses were reduced significantly over the course of obstruction. Markedly increased bladder weight and very large bladder volumes indicated decompensation. Nerve density was marked decreased in decompensated bladders. Similarly, SOD activity in muscle decreased progressively and was markedly lower in decompensated bladders. Although CAT activity of the muscle increased after 2-4 weeks of obstruction, it decreased markedly in decompensated bladders.
This study shows that prolonged PBOO causes progressive deterioration in the rabbit bladder with decompensation after 8 weeks. Markedly decreased nerve density and severely reduced SOD and CAT activities are associated with the shift from compensated to decompensated function of the bladder. They may be excellent biomarkers of decompensation.
膀胱出口部分梗阻(PBOO)会导致膀胱出现明显的收缩、生化及组织学改变。我们的目的是确定家兔渐进性PBOO的时间进程,并找到标志着失代偿转变的参数。
24只家兔接受1、2、4和8周的PBOO处理。假手术家兔作为对照。在每个时间段进行膀胱测压,并使用单个膀胱条进行收缩性研究。将每只家兔膀胱体的全层切片固定在福尔马林中,用于测定血管密度和神经密度。将膀胱体的肌肉和黏膜分离,分析超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的活性。
在梗阻过程中,膀胱重量逐渐增加,所有收缩反应均显著降低。膀胱重量显著增加和膀胱容量非常大表明出现失代偿。失代偿膀胱的神经密度显著降低。同样,肌肉中的SOD活性逐渐降低,在失代偿膀胱中显著降低。尽管梗阻2 - 4周后肌肉中的CAT活性增加,但在失代偿膀胱中显著降低。
本研究表明,长期PBOO会导致家兔膀胱逐渐恶化,8周后出现失代偿。神经密度显著降低以及SOD和CAT活性严重降低与膀胱从代偿功能向失代偿功能的转变有关。它们可能是失代偿的优秀生物标志物。