Hamanaka T, Bill A
Department of Physiology and Medical Biophysics, University of Uppsala, Sweden.
Exp Eye Res. 1988 Mar;46(3):323-41. doi: 10.1016/s0014-4835(88)80023-x.
The anterior chamber was perfused with alpha-chymotrypsin, 50 micrograms ml-1, in mock aqueous humor in cynomolgus monkeys. The enzyme caused a marked rise in outflow facility and had clear effects on the structure of the outflow routes for aqueous humor. The intertrabecular spaces in the iridocorneal chamber angle were wider than normal, the openings in the uveal and corneoscleral meshwork appeared enlarged, there was ballooning of the juxtacanalicular region and the inner wall of Schlemm's canal into the canal and also splitting of the inner wall of the canal. The trabecular cells appeared relaxed with most of the cell processes retracted, some broken. There were discontinuities in the cell membrane and blebs. Parts of the trabecular beams were denuded. Two days after the enzyme treatment the facility was in the normal range, no splits in the inner wall of Schlemm's canal we observed but many of the other changes in structure remained. The number of invaginations in the inner wall of Schlemm's canal was markedly reduced after 2-18 days. A second and third perfusion with alpha-chymotrypsin caused a rise in outflow facility similar to the first. Some morphological changes remained 163 days after enzyme treatment. Pilocarpine a few days after alpha-chymotrypsin treatment caused a marked increase in outflow facility. The results suggest that alpha-chymotrypsin affects the glycoproteins of the cell membrane and as a result causes disorganization of the cytoskeleton, loss of loose adhesions and breaks of cell processes. The rapid recovery of the resistance to outflow was probably due to healing of the splits in the inner wall of Schlemm's canal; a marked reduction in the number of cells with invaginations suggests that in addition there may have been a reduction in the number of transcellular pores in the inner wall of Schlemm's canal.
在食蟹猴的模拟房水中，用50微克/毫升的α-糜蛋白酶灌注前房。该酶使房水流出率显著升高，并对房水流出途径的结构产生明显影响。虹膜角膜房角的小梁间隙比正常宽，葡萄膜小梁网和角巩膜小梁网的开口似乎扩大，近小管区域和施莱姆管内壁向管腔内膨出，且施莱姆管内壁出现分裂。小梁细胞显得松弛，大多数细胞突起回缩，有些断裂。细胞膜有间断和小泡。部分小梁束裸露。酶处理两天后，流出率在正常范围内，未观察到施莱姆管内壁分裂，但许多其他结构变化仍然存在。施莱姆管内壁的内陷数量在2 - 18天后显著减少。第二次和第三次用α-糜蛋白酶灌注导致流出率升高，与第一次相似。酶处理163天后仍有一些形态学变化。α-糜蛋白酶处理几天后，毛果芸香碱使流出率显著增加。结果表明，α-糜蛋白酶影响细胞膜糖蛋白，从而导致细胞骨架紊乱、松散连接丧失和细胞突起断裂。流出阻力的快速恢复可能是由于施莱姆管内壁分裂的愈合；内陷细胞数量显著减少表明，此外施莱姆管内壁的跨细胞孔数量可能也减少了。
