Article

Increased urinary nerve growth factor as a predictor of persistent detrusor overactivity after bladder outlet obstruction relief in a rat model.

Department of Urology and Urological Science Institute, Yonsei University College of Medicine, Seoul, Korea.
The Journal of urology (impact factor: 4.02). 06/2010; 183(6):2440-4. DOI:10.1016/j.juro.2010.02.003 pp.2440-4
Source: PubMed

ABSTRACT We evaluated urinary nerve growth factor as a predictive factor for persistent detrusor overactivity after bladder outlet obstruction relief in a rat model.
A total of 50 female Sprague-Dawley(R) rats were divided into 2 groups, including 10 sham operated controls and 40 with bladder outlet obstruction. Obstruction was induced by partial urethral ligation and relieved by ligation removal after 3 weeks. Voided urine was collected before bladder outlet obstruction at time 1, 3 weeks after obstruction onset at time 2 and 3 weeks after obstruction relief at time 3. Cystometry was done in awake rats at times 2 and 3. Bladder tissue was harvested at time 3. Urinary and bladder tissue nerve growth factor was measured by enzyme-linked immunosorbent assay with results adjusted based on creatinine concentration.
In 16 rats in which detrusor overactivity disappeared after bladder outlet obstruction relief (group 1) urinary nerve growth factor/creatinine significantly increased from time 1 to 2 and significantly decreased from time 2 to 3 (p = 0.001 and 0.003, respectively). In 8 rats with persistent detrusor overactivity despite obstruction removal (group 2) urinary nerve growth factor/creatinine significantly increased from time 1 to 2 but did not change from time 2 to 3 (p = 0.012 and 0.123, respectively). These rats with persistent detrusor overactivity also had significantly higher urinary nerve growth factor/creatinine at time 1 than controls and group 1 (p = 0.015 and 0.005, respectively).
Changes in urinary nerve growth factor may reflect detrusor overactivity, as diagnosed on 2 consecutive cystometries. Increased urinary nerve growth factor before bladder outlet obstruction may predict persistent detrusor overactivity after obstruction relief.

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    Article: Function of the Cold Receptor (TRPM8) Associated with Voiding Dysfunction in Bladder Outlet Obstruction in Rats.
    Ji Hee Jun, Hyo Jin Kang, Mei Hua Jin, Hye Young Lee, Young Jae Im, Hyun Jin Jung, Sang Won Han
    [show abstract] [hide abstract]
    ABSTRACT: Bladder outlet obstruction (BOO) causes storage and voiding dysfunction in the lower urinary tract. We investigated the expression of transient receptor potential cation channel subfamily M member 8 (TRPM8) to evaluate the relationship between TRPM8 expression and overactive bladder (OAB) in a rat model of BOO. Fifty female Sprague-Dawley rats were divided into 4 groups; normal (n=10), normal-menthol (n=10), BOO (n=15), BOO-menthol (n=15). After 3 weeks, cystometry was performed by infusing physiological saline and menthol (3 mM) into the bladder at a slow infusion rate. The histological changes and expression of TRPM8 in the bladder were investigated by Masson's trichrome staining, immunofluorescence and reverse transcription-polymerase chain reaction. Cystometry showed that the intercontraction interval (ICI; 428.2±23.4 vs. 880.4±51.2, P<0.001), micturition pressure (MP; 25.7±1.01 vs. 71.80±3.01, P<0.001), and threshold pressure (2.9±0.25 vs. 9.2±1.58, P<0.01) were significantly increased in BOO rats. The bladder wall was significantly dilated compared with the control. Detrusor muscle hypertrophy and a thick mucosa layer were observed in BOO bladder. After menthol treatment, ICIs were decreased and MPs were increased in the menthol treatment groups. TRPM8-positive cells and mRNA were predominantly increased in the bladder and dorsal root ganglia of all groups compared with the normal group. Increased bladder wall thickness and proportion of collagen probably affect voiding dysfunction. Furthermore, an increase of TRPM8 expression in BOO may induce entry of Ca(2+) from the extracellular space or stores. The increase of Ca(2+) probably causes contraction of smooth muscle in BOO. However, OAB symptoms were not observed after menthol treatment although the expression of TRPM8 was abundant in the bladder epithelium after menthol treatment. Although OAB in BOO models may be caused by complex pathways, regulation of TRPM8 presents possibilities for OAB treatment.
    International neurourology journal 06/2012; 16(2):69-76.
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Keywords

2 consecutive cystometries
 
2 groups
 
3 weeks
 
50 female Sprague-Dawley(R)
 
bladder outlet obstruction
 
bladder outlet obstruction relief
 
Bladder tissue
 
creatinine concentration
 
enzyme-linked immunosorbent assay
 
group 1
 
group 2
 
Increased urinary nerve growth factor
 
partial urethral ligation
 
persistent detrusor overactivity
 
time 1
 
time 2
 
time 3. Cystometry
 
time 3. Urinary
 
times 2
 
urinary nerve growth factor