Involvement of purinergic neurotransmission in ketamine induced bladder dysfunction.
J Urol
; 186(3): 1134-41, 2011 Sep.
Article
em En
| MEDLINE
| ID: mdl-21784472
ABSTRACT
PURPOSE:
Long-term ketamine abuse in humans causes significant lower urinary tract symptoms. However, the etiology of ketamine associated cystitis is still not clear. We created a mouse model of ketamine induced lower urinary tract dysfunction to explore the pathogenesis of this condition. MATERIALS ANDMETHODS:
Female C57BL/6 mice randomly distributed into control and ketamine groups received daily intraperitoneal injection of saline and ketamine (100 mg/kg), respectively. Cystometry was done in each group at 4, 8 and 16 weeks. After sacrifice the bladders were harvested for isometric muscle tension recording and immunohistochemical examination.RESULTS:
After 8 weeks of treatment body weight growth was significantly decreased in ketamine treated mice. Cystometry revealed a significantly decreased intercontraction interval (mean±SEM 237±9 vs 360±20 seconds, p<0.001) and decreased bladder capacity (0.1±0.004 vs 0.13±0.006 ml, p<0.001) in ketamine vs saline injected mice. Increased adenosine triphosphate evoked detrusor contraction developed in the ketamine group. Immunohistochemical examination revealed increased P2X1 receptor expression in ketamine treated mouse bladders while M2 and M3 receptor expression was unchanged.CONCLUSIONS:
At 8 weeks mice treated with ketamine showed increased voiding frequency and decreased bladder capacity, the same symptoms that develop in human ketamine abusers. Enhanced noncholinergic contractions and P2X1 receptor expression in the ketamine bladder indicate that dysregulation of purinergic neurotransmission may underlie detrusor overactivity in cases of ketamine induced bladder dysfunction.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Doenças da Bexiga Urinária
/
Receptores Purinérgicos
/
Transmissão Sináptica
/
Ketamina
Limite:
Animals
Idioma:
En
Ano de publicação:
2011
Tipo de documento:
Article