Effect of several drugs on disruption of blood-aqueous barrier

血-房水屏障的破坏使前房中的蛋白质和闪光升高。PGE 2、PGE 2受体拮抗剂和异丙基乌诺前列酮（PG相关抗青光眼药物）破坏了有色兔的血-房水屏障。他洛尔（具有钙阻断活性的抗青光眼剂）、阿普拉尼定（α 2激动剂），肾上腺素（β 2拮抗剂），diviyefrin（β 2拮抗剂），倍他米松（皮质类固醇），氟米龙（皮质类固醇）、双氯芬酸（非甾体抗炎药），普拉洛芬（非甾体抗炎药），黄芩素黄芩苷（一种从草药中分离出来的成分）（从草药中分离的成分），曲马唑啉（血管构造剂）、FR 122047（考克斯-1抑制剂）和FR 188582（考克斯-2抑制剂）抑制了色素兔中PGE 2诱导的房水闪光升高。白内障患者的Kakkon-to或青光眼患者的倍他洛尔可抑制术后房水闪光升高。这些药物可能用于治疗葡萄膜炎。

Disruption of blood-aqueous barrier elevates protein and flare in the anterior chamber. PGE2,PGE2 receptor antagonist, and isopropyl unoprostone (PG-related antiglaucoma agent) disrupted the blood -aqueous barrier in pigmented rabbits. Betaxolol (antiglaucoma agent having calcium blocking activity), apraclonidine (α 2 agonist), epinephrine (β 2 antagonist), diviyefrin (β 2 antagonist), betamethasone (corticosteroid), fluorometholone (corticosteroid), diclofenac (non-steroidal anti-inflammatory drug), pranoprofen (non-steroidal anti-inflammatory drug), baicalein (a component isolated from medicinal herb), baicalin (a component isolated from medicinal herb), tramazoline (vasoconstructor), FR122047 (COX-1 inhibitor), and FR188582(COX-2 inhibitor) suppressed PGE2-induced aqueous, flare elevation in pigmented rabbits. Postoperative aqueous flare elevation was inhibited by Kakkon-to in cataract patients or by betaxolol in glaucoma patients. It is possible that these agents may be useful in treatment for uveitis.