大肠杆菌内毒素诱导的SD大鼠眼内炎

目的 观察细菌内毒素脂多糖(LPS)诱导的大鼠眼内炎性反应的临床、组织病理学和血眼屏障的特点.方法 SD大鼠玻璃体腔内注人大肠杆菌LPS(1μg)建立LPS诱导的眼内炎动物模型,对照组注入无菌生理盐水.在LPS注入后6h至7d的不同时点,分别对眼部炎性反应评分、浸润白细胞计数、前房水蛋白质浓度和玻璃体内LPS水平进行测定和评估.结果 在LPS注射后6～72 h眼内可见严重的炎性反应,至术后7d炎性反应基本消退.眼内白细胞的浸润数量在术后24h达到高峰[(1182.63±191.15)细胞/眼],至术后3 d浸润细胞数量迅速下降[(331.25±57.9)细胞/眼].在各观察时点,均可观察到眼内炎组房水蛋白质浓度较对照组显著增高(P<0.01). LPS注入眼内后前3 d,玻璃体腔内LPS含量迅速下降[前3d分别为(327.02±51.54)、(176.0±53.68)和(54.91±13.26)ng],在7d后玻璃体腔内LPS基本被清除.结论 大肠杆菌内毒素在SD大鼠可诱导出严重的实验性眼内炎,大量白细胞眼内浸润、血眼屏障破坏和玻璃体腔自发性细菌成分清除是本实验性眼内炎模型的主要病理特点.

Characteristics of endophthalmitis induced by endotoxin from Escherichia coli in Sprague - Dawley rats

Objective To study the clinical, histopathologic features and to determine the blood-ocular barrier change of endotoxin lipopolysaccharide (LPS) induced endophthalmitis in rats.Methods Experimental Sprague-Dawley rats received an intravitreal injection of LPS from Escherichia coli (1 μg), and control rats received sterile saline.The clinical scores, cellular infiltrate, protein concentration in aqueous humor and LPS concentration in vitreous, were measured and compared at different time points from 6 hours to 7 days after LPS injection.Results Severe inflammatory responses in the eyes were observed in rats between 6 and 72 hours after LPS injection.Ocular inflammation resolved by day 7.In the vitreous, a peak neutrophil count was observed at 24 h [(1182.63±191.15) cells/eye] that rapidly declined by day 3[(331.25± 57.9) cells/eye].Significant higher protein in aqueous humor compared with that in saline-control group was found in LPS-treated group at all time points (P<0.01).Eyes injected with LPS showed LPS level in the vitreous decreased rapidly in the first 3 days [(327.02±51.54), (176.0±53.68) and (54.91 ± 13.26) ng, respectively] and disappeared at day 7.Conclusions Experimental endophthalmitis with marked clinical signs is successfully induced in the Sprague-Dawley rats with intravitreal injection of lipopolysaccharide from Escherichia coli.Massive neutrophils infiltration, blood- ocular barrier breakdown and spontaneous elimination of bacterial elements are major pathological characteristics in this experimental model.