The timing of established detrusor hyperreflexia in a rat model of neuropathic bladder.

BACKGROUND: Proper timing of catheter insertion and the use of a suitable surgical method are essential parts of producing rat models to evaluate neuropathic bladder following spinal cord injury (SCI). METHODS: Thirty-two female Sprague-Dawley rats were randomly allocated into four groups. Group 1 underwent surgical laminectomy using the classic method. Group 2 underwent SCI 7 d following insertion of the catheter, and group 3 underwent sham operation. For bladder catheterization, a 4.5 Fr catheter was fixed into the bladder and tunneled beneath the skin to reach out at the nape of the neck. Group 4 underwent urodynamic study via bladder catheter prior to surgery and every 10 d following the operation to determine the exact time of establishing neuropathic bladder following spinal shock. The animals' survival rate and bladder wall's histopathologic changes were assessed 30 d following the operation. RESULTS: Simultaneous suprapubic catheter placement raised the mortality rate in group 1 in comparison with group 2. Repeated urodynamic study in group 4 showed hypertonic behavior in the bladder 10 d after SCI, with significantly increased leak point pressure and bladder capacity; however, the end filling pressure and constant neuropathic bladder on cystometric indices are attained from 20 d after the operation. CONCLUSIONS: Insertion of a bladder catheter 1 wk prior to SCI provides an applicable route for repeated cystometric studies in rats. The results demonstrate that sustained bladder overactivity is established in rats 20 d after SCI and animals are ready for further experiments on neuropathic bladder dysfunction following this period.

Chronic lithium administration ameliorates 2,4,6-trinitrobenzene sulfonic acid-induced colitis in rats; potential role for adenosine triphosphate sensitive potassium channels.

BACKGROUND AND AIM: Inflammatory bowel disease (IBD) is a multi-factorial disease with an unknown etiology characterized by oxidative stress, leukocyte infiltration and a rise in inflammatory cytokines. This study was conducted to investigate lithium in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced chronic model of experimental IBD, and the contribution of potassium channels as a possible underlying mechanism. METHODS: Experimental IBD was induced in rats by a single colonic administration of 10 mg of TNBS. Lithium, Glibenclamide (a potassium channel blocker), Lithium + Glibenclamide, Cromakalim or Lithium+Glibenclamide+ Cromakalim were given twice daily for 7 successive days. At the end of the experiment, macroscopic and histopathologic scores, colonic malondialdehyde (MDA), tumor necrosis factor-α (TNF-α) level, and myeloperoxidase (MPO) activity as well as plasma lithium level were assessed. RESULTS: Both macroscopic and histological features of colonic injury were markedly ameliorated by lithium. Likewise, the elevated amounts of MPO and MDA were diminished as well as those of TNF-α (P < 0.05). Glibenclamide reversed the effect of lithium on these markers, Addition of cromakalim abrogated the effects mediated by glibenclamide and markedly decreased MPO activity, MDA level and TNF-α content (P < 0.0.05). Macroscopic and microscopic scores and biochemical markers were significantly decreased in Cromakalim-treated animals. No significant difference was observed between TNBS and Glibenclamide groups. CONCLUSION: Lithium exerts prominent anti-inflammatory effects on TNBS-induced colitis in rats. Potassium channels contribute to these beneficial properties.