Department of Psychology, University of Alabama at Birmingham, AL 35205, USA.
J Pain. 2010 Mar;11(3):247-55. doi: 10.1016/j.jpain.2009.07.010. Epub 2009 Nov 27.
Neonatal bladder inflammation has been demonstrated to produce hypersensitivity to bladder re-inflammation as an adult. The purpose of this study was to investigate the effects of neonatal urinary bladder inflammation on adult bladder function and structure. Female Sprague-Dawley rats were treated on postnatal days 14 to 16 with intravesical zymosan or anesthesia alone. At 12 to 16 weeks of age, micturition frequency and cystometrograms were measured. Similarly treated rats had their bladders removed for measurement of plasma extravasation after intravesical mustard oil, for neuropeptide analysis (calcitonin gene-related peptide or Substance P) or for detailed histological examination. Rats treated with zymosan as neonates exhibited increased micturition frequency, reduced micturition volume thresholds, greater extravasation of Evans blue after intravesical mustard oil administration, and greater total bladder content of calcitonin gene-related peptide and Substance P. In contrast, there were no quantitative histological changes in the thickness, fibrosis, or mast cells of bladder tissue due to neonatal zymosan treatments. Functional changes in urologic systems observed in adulthood, coupled with the increased neuropeptide content and neurogenic plasma extravasation in adult bladders, suggest that the neonatal bladder inflammation treatment enhanced the number, function, and/or neurochemical content of primary afferent neurons. These data support the hypothesis that insults to the urologic system in infancy may contribute to the development of adult bladder hypersensitivity.
Inflammation of the bladder early in life in the rat has multiple sequelae, including laboratory measures that suggest an alteration of the neurophysiological substrates related to the bladder. Some painful bladder syndromes in humans have similar characteristics and so may be due to similar mechanisms.
已证实新生儿膀胱炎症会导致成年后对膀胱再炎症产生过敏反应。本研究旨在探讨新生儿膀胱炎症对成年后膀胱功能和结构的影响。雌性 Sprague-Dawley 大鼠在出生后第 14 至 16 天接受膀胱内酵母聚糖或单独麻醉处理。在 12 至 16 周龄时，测量排尿频率和膀胱测压图。同样接受处理的大鼠在膀胱内芥子油给药后，测量血浆外渗以进行神经肽分析（降钙素基因相关肽或 P 物质）或进行详细的组织学检查，然后切除膀胱。新生鼠接受酵母聚糖处理后，排尿频率增加，排尿量阈值降低，膀胱内芥子油给药后 Evans 蓝外渗增加，降钙素基因相关肽和 P 物质在整个膀胱中的含量增加。相比之下，由于新生鼠接受酵母聚糖处理，膀胱组织的厚度、纤维化或肥大细胞无明显的定量组织学变化。成年期观察到的泌尿系统功能变化，以及成年期膀胱中神经肽含量增加和神经源性血浆外渗，表明新生儿膀胱炎症处理增强了初级传入神经元的数量、功能和/或神经化学含量。这些数据支持这样一种假说，即婴儿期泌尿系统的炎症可能导致成年后膀胱过敏反应的发展。
大鼠生命早期的膀胱炎症有多种后遗症，包括实验室测量提示与膀胱相关的神经生理底物发生改变。一些人类的膀胱疼痛综合征具有类似的特征，因此可能与类似的机制有关。
