Imamura Tetsuya, Ishizuka Osamu, Aizawa Naoki, Zhong Chen, Ogawa Teruyuki, Nakayama Tsuyoshi, Tanabe Tomoaki, Nishizawa Osamu
Department of Urology, Shinshu University School of Medicine, Matsumoto Nagano, Japan.
Neurourol Urodyn. 2008;27(4):348-52. doi: 10.1002/nau.20497.
We determined if cold environmental stress induced detrusor overactivity in conscious rats. We then examined the role of resiniferatoxin (RTX)-sensitive nerves in this response.
Three days prior to cystometric investigation, the urinary bladders of 12 female rats were cannulated. Six of the rats were treated with RTX 24 hr prior to cystometric investigation. The rats were exposed to three ambient temperature conditions: room temperature (RT, 27 degrees C) for 20 min, low temperature (LT, 4 degrees C) for 40 min, and RT again for 20 min. During each exposure, cystometric patterns of the rats were recorded. Additionally, neuronal structures of urinary bladders were visualized by immunohistochemistry.
When the conscious rats were suddenly transferred from RT to LT, the cooled rats exhibited micturition patterns of detrusor overactivity. After 20 min at LT, the response slowly improved. After returning to RT, the overactive detrusor response disappeared, reverting to patterns similar to those before transfer to LT. When the RTX-treated rats were exposed with cold stress, they also exhibited detrusor overactivity. However, it was significantly mitigated compared to the non-RTX-treated normal rats. The normal rats had distinct neuronal structures labeled with S100 and calcitonin gene-related peptide antibodies in the urinary bladders, but the RTX-treated rats had few.
Detrusor overactivity of the conscious rats was induced by cold environmental stress. A portion of the cold-stress detrusor overactivity might be mediated by RTX-sensitive neurological pathway. The cold-stress model would be useful to investigate lower urinary tract functions.
我们确定寒冷环境应激是否会在清醒大鼠中诱发逼尿肌过度活动。然后我们研究了树脂毒素(RTX)敏感神经在这一反应中的作用。
在膀胱测压研究前三天,对12只雌性大鼠的膀胱进行插管。其中6只大鼠在膀胱测压研究前24小时接受RTX治疗。将大鼠暴露于三种环境温度条件下:室温(RT,27℃)20分钟、低温(LT,4℃)40分钟,然后再次在室温下20分钟。在每次暴露期间,记录大鼠的膀胱测压模式。此外,通过免疫组织化学观察膀胱的神经元结构。
当清醒大鼠突然从室温转移到低温环境时,受冷大鼠表现出逼尿肌过度活动的排尿模式。在低温环境下20分钟后,这种反应逐渐改善。回到室温后,逼尿肌过度活动反应消失,恢复到与转移到低温环境前相似的模式。当用RTX处理的大鼠受到冷应激时,它们也表现出逼尿肌过度活动。然而,与未用RTX处理的正常大鼠相比,这种活动明显减轻。正常大鼠膀胱中有明显的用S100和降钙素基因相关肽抗体标记的神经元结构,但用RTX处理的大鼠则很少。
寒冷环境应激可诱发清醒大鼠的逼尿肌过度活动。冷应激诱发的部分逼尿肌过度活动可能由RTX敏感的神经通路介导。冷应激模型将有助于研究下尿路功能。