Çelebi Süleyman, Kuzdan Özgür, Özaydın Seyithan, Başdaş Cemile Beşik, Özaydın İpek, Erdoğan Cankat, Sander Serdar
Department of Pediatric Urology, Kanuni Sultan Suleyman Education and Research Hospital, Istanbul, Turkey.
Department of Pediatric Surgery, Kanuni Sultan Suleyman Education and Research Hospital, Istanbul, Turkey.
J Pediatr Urol. 2016 Oct;12(5):311.e1-311.e6. doi: 10.1016/j.jpurol.2016.03.010. Epub 2016 Apr 16.
Shuttling of some of the bladder volume into the bladder diverticulum (BD) can cause urinary retention, lower urinary tract dysfunction, infection, and stone formation. This experimental study is the first to create a rabbit BD to study micturition physiology (urodynamics and pathology) that mimics clinical findings.
The study included 16 New Zealand adult male rabbits in the BD group and 16 sham-operated controls. BD creation consisted of a lower midline laparotomy and bladder entry via the spacing between the detrusor muscle fibers and the mucosa, posterolaterally from the bladder wall. The detrusor was excised to provide a mucosal prolapsus, creating a narrow BD neck (Figure). The sham group underwent bladder exposure with a midline incision. All rabbits underwent urodynamic study preoperatively and postoperatively, consisting of postmicturition residue (PMR), maximum bladder capacity (MBC), voiding detrusor pressure (VPdet), filling detrusor pressure (FPdet), compliance, and urine flow (Qflow). The animals were then sacrificed and their bladders assessed for pathology and stone formation.
Preoperative MBC, Pdet, and Qmax were within reference ranges. No animals had PMR or urinary tract infections (UTIs). The BD group showed urodynamic and pathologic bladder changes, including decreased (28%) cystometric bladder capacity and compliance (Sham: 26.8 ± 0.4; BD: 4.46 ± 1.08, p = 0.0001) and increased post-void residual PMR (8.3 ± 2.4 mL). Pathology revealed increased bladder detrusor thickness correlated with urodynamic findings of increased filling detrusor pressures (Sham: 1.58 ± 0.2; BD: 4.89 ± 0.93, p = 0.0001). Urodynamics revealed intermittent BD bladder contraction during the filling phases. Eight BD group rabbits had UTIs; five had stone formation (4-9 mm).
In the literature, it has not been determined whether lower urinary tract disorders (LUTD) could cause diverticula, or if a congenital diverticula could be reason for LUTD. Anatomical or neurological reasons for a low-compliance bladder can cause diverticulosis. As demonstrated in our study with rabbits, the congenital diverticulum could further reduce the compliance of the bladder. Further, a decrease in compliance logically correlates with the progressive decompensation of the bladder.
The nature of diverticula remains undetermined. All the information presented for this model is relevant to our clinical observations. We conclude that the rabbit bladder can be used for research into experimental diverticulum-induced changes in the activity of the bladder and for experimental detrusor research.
部分膀胱容量进入膀胱憩室（BD）可导致尿潴留、下尿路功能障碍、感染和结石形成。本实验研究首次创建兔BD以研究模拟临床发现的排尿生理学（尿动力学和病理学）。
本研究包括16只新西兰成年雄性兔作为BD组和16只假手术对照组。创建BD包括下腹正中剖腹术，并通过膀胱壁后外侧逼尿肌纤维与黏膜之间的间隙进入膀胱。切除逼尿肌以形成黏膜脱垂，形成狭窄的BD颈部（图）。假手术组通过正中切口暴露膀胱。所有兔在术前和术后均接受尿动力学研究，包括排尿后残余尿量（PMR）、最大膀胱容量（MBC）、排尿时逼尿肌压力（VPdet）、充盈时逼尿肌压力（FPdet）、顺应性和尿流率（Qflow）。然后处死动物并评估其膀胱的病理学和结石形成情况。
术前MBC、Pdet和Qmax在参考范围内。没有动物出现PMR或尿路感染（UTI）。BD组显示尿动力学和病理性膀胱改变，包括膀胱容量和顺应性降低（28%）（假手术组：26.8±0.4；BD组：4.46±1.08，p = 0.0001）以及排尿后残余尿量PMR增加（8.3±2.4 mL）。病理学显示膀胱逼尿肌厚度增加与充盈时逼尿肌压力增加的尿动力学结果相关（假手术组：1.58±0.2；BD组：4.89±0.93，p = 0.0001）。尿动力学显示在充盈期BD膀胱间歇性收缩。BD组8只兔发生UTI；5只出现结石形成（4 - 9 mm）。
在文献中，尚未确定下尿路疾病（LUTD）是否可导致憩室，或者先天性憩室是否可能是LUTD的原因。膀胱顺应性降低的解剖学或神经学原因可导致憩室病。如我们在兔研究中所示，先天性憩室可进一步降低膀胱顺应性。此外，顺应性降低在逻辑上与膀胱的进行性失代偿相关。
憩室的性质尚未确定。该模型提供的所有信息与我们的临床观察相关。我们得出结论，兔膀胱可用于研究实验性憩室引起的膀胱活动变化以及实验性逼尿肌研究。
