Ito Y, Sugatani J, Miki H, Uyama M, Saito K
Department of Ophthalmology, Kansai Medical University, Osaka, Japan.
Exp Eye Res. 1993 Jul;57(1):107-15. doi: 10.1006/exer.1993.1104.
The involvement of platelet-activating factor (PAF) in the development of anterior segment necrosis after occlusion of the bilateral long posterior ciliary arteries was investigated in rabbits. With the progression of anterior segment necrosis, which was characterized by corneal edema and neovascularization, the contents of protein and total phospholipids increased in the cornea and aqueous humor, but not in the iris. PAF acetylhydrolase activity was significantly increased on the first postoperative day in the peripheral cornea and on the second day in the central cornea prior to the development of marked corneal edema and neovascularization, but it did not increase in the iris. The accumulation of newly synthesized PAF in the cornea reached a plateau level on the third postoperative day, which coincided with the progression of the corneal lesion. In the aqueous humor, PAF acetylhydrolase activity was increased by the induced ischemia, but no PAF was detected. The increased PAF acetylhydrolase activity may reflect adaptation to the participation of PAF in the progression of anterior segment necrosis.
在兔身上研究了血小板活化因子(PAF)在双侧睫状后长动脉闭塞后眼前节坏死发展过程中的作用。随着眼前节坏死的进展,其特征为角膜水肿和新生血管形成,角膜和房水中蛋白质和总磷脂含量增加,但虹膜中未增加。在明显的角膜水肿和新生血管形成之前,术后第一天外周角膜和第二天中央角膜的PAF乙酰水解酶活性显著增加,但虹膜中未增加。角膜中新合成的PAF在术后第三天达到平台期,这与角膜病变的进展相一致。在房水中,诱导缺血可增加PAF乙酰水解酶活性,但未检测到PAF。PAF乙酰水解酶活性增加可能反映了对PAF参与眼前节坏死进展的适应性变化。