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通过暴露于硫酸鱼精蛋白后再给予细菌内毒素在大鼠中诱导建立膀胱损伤模型。

Bladder injury model induced in rats by exposure to protamine sulfate followed by bacterial endotoxin.

作者信息

Stein P C, Pham H, Ito T, Parsons C L

机构信息

Department of Surgery, University of California San Diego 92103-8897, USA.

出版信息

J Urol. 1996 Mar;155(3):1133-8.

PMID:8583579
Abstract

PURPOSE

A bladder injury model was developed using protamine sulfate (PS) and endotoxin lipopolysaccharide (LPS) administered intravesically to female Sprague-Dawley rats.

MATERIALS AND METHODS

Experimental and control animals were catheterized and intravesically exposed to PS-LPS, PS, LPS, or phosphate buffered saline. After 4, 24 or 72 hours, rats were sacrificed. Urines and bladder tissues were then obtained. Bladder mucosal permeability was evaluated by measuring 14C-urea uptake 24 hours after injury. Repeated instillations of PS/LPS were also made in another group of rats over a period of 5 weeks to attempt to establish a more serious mucosal injury, possibly reflected by altered staining of the collagen IV component of the urinary basement membrane (UBM).

RESULTS

Histological examination of the tissues indicated a maximal inflammatory response in the mucosa 4 hours after instillation of PS/LPS. Neutrophils and macrophages in close proximity to the UBM and intraepithelially could be demonstrated. Bladder permeability was significantly altered (26.9% 14C-urea uptake) in rats assayed 24 hours after the PS/LPS treatment, but not after exposure to PS or LPS alone (11.9 and 17.5%, respectively). Protease activity detected in urines from experimental, but not control, animals coincided with the appearance of inflammatory cells in the lamina propria. Inflammatory injury did not appear to alter the collagen IV staining of the UBM.

CONCLUSIONS

This rat bladder injury model is useful for examining controversial issues regarding bladder wall structure-function alterations induced by inflammation and possibly important in the pathobiological mechanisms involved in some patients with interstitial cystitis.

摘要

目的

通过向雌性Sprague-Dawley大鼠膀胱内注射硫酸鱼精蛋白(PS)和内毒素脂多糖(LPS)建立膀胱损伤模型。

材料与方法

将实验动物和对照动物进行插管,并膀胱内给予PS-LPS、PS、LPS或磷酸盐缓冲盐水。4、24或72小时后处死大鼠,然后获取尿液和膀胱组织。通过测量损伤后24小时的14C-尿素摄取来评估膀胱黏膜通透性。在另一组大鼠中,在5周的时间内反复滴注PS/LPS,试图建立更严重的黏膜损伤,这可能通过尿基底膜(UBM)IV型胶原成分染色改变得以体现。

结果

组织学检查显示,在PS/LPS滴注后4小时,黏膜出现最大程度的炎症反应。可证实靠近UBM和上皮内有中性粒细胞和巨噬细胞。PS/LPS处理后24小时检测的大鼠膀胱通透性显著改变(14C-尿素摄取率为26.9%),但单独暴露于PS或LPS后未出现这种情况(分别为11.9%和17.5%)。在实验动物而非对照动物的尿液中检测到的蛋白酶活性与固有层中炎症细胞的出现一致。炎症损伤似乎未改变UBM的IV型胶原染色。

结论

该大鼠膀胱损伤模型有助于研究关于炎症诱导的膀胱壁结构-功能改变的争议性问题,并且可能在一些间质性膀胱炎患者的病理生物学机制中具有重要意义。

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