Mild Brain Ischemia Produces Bladder Hyperactivity without Brain Damage in Rats
Mild Brain Ischemia Produces Bladder Hyperactivity without Brain Damage in Rats
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DOI：
10.1159/000092936
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发表时间：
2006-07
影响因子：
1.6
通讯作者：
S. Yotsuyanagi;K. Narimoto;M. Namiki
中科院分区：
文献类型：
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作者：
S. Yotsuyanagi;K. Narimoto;M. Namiki
简介：不伴脑梗塞的脑缺血对排尿功能的影响尚不清楚。为了研究脑血流量减少对排尿功能的影响，研究了慢性脑灌注不足（CH）对大鼠膀胱活动的影响。材料和方法：11 只雌性 Sprague-Dawley 大鼠通过右颈外静脉与右颈总动脉吻合，部分阻塞左颈总动脉，诱导 CH。十二只完整的动物组成对照组。在第 2、4 和 8 周，在代谢笼中评估每次排尿的排尿量 24 小时。术后八周，在海马体相关的学习模式（莫里斯水迷宫）中对大鼠进行测试。 2 周时通过连续输注膀胱内压描记术 (CMG) 监测 13 只大鼠的膀胱活动。评估后，用2% 2,3,5-三苯基氯化四唑（TTC）灌注对大鼠脑进行染色。结果：与对照组相比，CH 后 2 周，CH 大鼠每次排尿的排尿量显着减少，排尿频率显着增加（p < 0.05）。与对照组相比，CH 大鼠的 CMG 膀胱容量在 CH 后 14 天显着降低（p < 0.05）。尽管CH大鼠大脑的TTC染色未显示脑梗塞，但CH引起了水迷宫学习障碍。结论：这些结果表明，没有梗塞的轻度前脑缺血会导致膀胱过度活跃和记忆障碍。衰老引起的轻度脑缺血可能会导致人类膀胱过度活动。使用该动物模型对与膀胱过度活动相关的神经系统进行进一步研究可能会导致对具有不明原因的排尿功能障碍的老年人进行药物治疗或预防膀胱过度活动。
Introduction: The influence of brain ischemia without cerebral infarction on voiding function is unknown. To investigate the effects of a reduction in cerebral blood flow on voiding function, the influence of chronic cerebral hypoperfusion (CH) on bladder activity was examined in rats. Materials and Methods: CH was induced in each of 11 female Sprague-Dawley rats by anastomosis between the right external jugular vein and the right common carotid artery with partial obstruction of the left common carotid artery. Twelve intact animals comprised a control group. Voided volume per micturition was assessed in a metabolic cage for 24 h on weeks 2, 4, and 8. Eight weeks after the operation, the rats were tested in a hippocampus-related learning paradigm, the Morris water maze. Bladder activity was monitored in 13 rats with continuous infusion cystometrography (CMG) at 2 weeks. After evaluation, the rats’ brains were stained by perfusion with 2% 2,3,5-triphenyltetrazolium chloride (TTC). Results: Voided volume per micturition was significantly reduced and voiding frequency was significantly increased in CH rats 2 weeks after CH as compared to the control group (p < 0.05). Bladder capacity on CMG of CH rats was significantly reduced 14 days after CH as compared to the controls (p < 0.05). Although TTC staining of the CH rat brain did not show cerebral infarction, CH induced impairment of water maze learning. Conclusions: These results indicate that mild forebrain ischemia without infarction results in the development of bladder hyperactivity and impairment of memory. Mild brain ischemia with aging may induce bladder overactivity in humans. Further studies of the nervous system related to bladder hyperactivity using this animal model may lead to pharmacological therapy or prevention of bladder overactivity in the aging individual with an unidentified origin of voiding dysfunction.