Ruiz-Moreno J M, Misiuk-Hojlo M, Thillaye B, de Kozak Y
Laboratoire d'Immunopathologie de l'Oeil, INSERM U 86, Paris, France.
Curr Eye Res. 1992;11 Suppl:135-40. doi: 10.3109/02713689208999523.
S-antigen (S-Ag)-induced experimental autoimmune uveoretinitis (EAU) was suppressed in Lewis and PVG rats by treatment beginning 4 days post immunization with prazosin, a specific alpha 1-adrenergic receptor antagonist. A significant suppression of EAU was observed at clinical and histological levels in both treated groups compared to a severe EAU which developed in controls. Fluorescein angiography showed no leakage of dye from the optic disc of a treated PVG rat presenting no ocular inflammation by clinical examination. The treatment had no effect on the titer of anti-S-Ag antibodies. Perivascular infiltrates of T-lymphocytes and macrophages together with alterations of blood-retinal barrier permeability are early events in EAU. Prazosin, by acting on the vascular alpha 1-adrenoreceptors, inhibits vasospasm, preserves blood-retinal-barrier integrity and prevents vascular edema and early inflammatory cell infiltration observed in EAU.
在Lewis和PVG大鼠中，通过在免疫后4天开始用特异性α1 - 肾上腺素能受体拮抗剂哌唑嗪治疗，可抑制S - 抗原（S - Ag）诱导的实验性自身免疫性葡萄膜视网膜炎（EAU）。与对照组中发展为严重EAU相比，两个治疗组在临床和组织学水平均观察到EAU受到显著抑制。荧光素血管造影显示，经临床检查无眼部炎症的治疗后PVG大鼠的视盘无染料渗漏。该治疗对抗S - Ag抗体滴度无影响。T淋巴细胞和巨噬细胞的血管周围浸润以及血视网膜屏障通透性的改变是EAU的早期事件。哌唑嗪通过作用于血管α1 - 肾上腺素能受体，抑制血管痉挛，保持血视网膜屏障完整性，并预防EAU中观察到的血管水肿和早期炎症细胞浸润。
