Cousins S W, Guss R B, Howes E L, Rosenbaum J T
Exp Eye Res. 1984 Nov;39(5):665-76. doi: 10.1016/0014-4835(84)90065-4.
A single intraperitoneal dose of endotoxin (lipopolysaccharide or LPS) induces an acute inflammatory response in the uveal tract of rats. This inflammation is characterized by a breakdown of the blood/aqueous barrier within 3 hr after the LPS and the subsequent development of clinical disease and a cellular infiltrate. Early change in vascular permeability, clinical, and pathological changes were dose dependent with the two highest doses (100 micrograms or 500 micrograms) producing more severe pathology. Clinical and histopathologic abnormalities peaked at 24 hr and were resolving by 48 hr. Although clinical and histologic changes correlated well, the degree of breakdown of the blood/aqueous barrier at 3 hr failed to predict the extent of the cellular exudate measured by either clinical or histologic criteria. In addition, pharmacologic suppression of the early vascular permeability changes with indomethacin, cyproheptadine, or both agents failed to protect the animals consistently from subsequently developing significant clinical disease or cellular infiltrates on histopathology. LPS-induced uveitis in the rat provides a simple, reproducible model for ocular inflammation without requiring direct eye manipulation. The mediators responsible for the early vascular permeability in this model appear to be distinct from the mediators primarily responsible for the subsequent cellular exudate.
腹腔内单次注射内毒素（脂多糖或LPS）可在大鼠葡萄膜诱导急性炎症反应。这种炎症的特征是在注射LPS后3小时内血-房水屏障破坏，随后出现临床疾病和细胞浸润。血管通透性的早期变化、临床和病理变化呈剂量依赖性，两种最高剂量（100微克或500微克）产生更严重的病理改变。临床和组织病理学异常在24小时达到峰值，并在48小时时消退。虽然临床和组织学变化相关性良好，但3小时时血-房水屏障的破坏程度未能预测通过临床或组织学标准测量的细胞渗出程度。此外，用吲哚美辛、赛庚啶或两种药物对早期血管通透性变化进行药理抑制，不能始终保护动物免于随后出现显著的临床疾病或组织病理学上的细胞浸润。大鼠LPS诱导的葡萄膜炎提供了一种简单、可重复的眼部炎症模型，无需直接眼部操作。该模型中负责早期血管通透性的介质似乎与主要负责随后细胞渗出的介质不同。
