Olsen T
Acta Ophthalmol (Copenh). 1980 Apr;58(2):257-66. doi: 10.1111/j.1755-3768.1980.tb05719.x.
In order to assess a possible damage to the corneal endothelium during pressure induced abnormal hydration of the cornea, 23 patients with a previous attack of unilateral acute glaucoma were photographed with a specular microscope. As compared to the healthy side, the endothelium of the affected side showed a mean decrease in cell density of 23.1%, range --4.8 to 68% (P less than 0.001). In retrospect this cell loss was found to correlate significantly to the increase in corneal thickness measured during the acute attack on first day of admission. At present examination mean central corneal thickness was identical in the affected and unaffected eye. A large variation was, however, found in the intraocular pressure of the previously attacked eye. If the subject inter-eye difference in intraocular pressure was related to the inter-eye difference in corneal thickness is significant negative correlation appeared. It is concluded that the intraocular pressure has a dual effect on the corneal hydration: if the endothelium is intact, the intraocular pressure decreases corneal thickness, whereas an increase is seen only if the endothelium is acutely damaged.
为了评估在压力诱导的角膜异常水化过程中角膜内皮可能受到的损伤,用镜面显微镜对23例既往有单侧急性青光眼发作史的患者进行了拍照。与健侧相比,患侧内皮细胞密度平均降低23.1%,范围为-4.8%至68%(P<0.001)。回顾发现,这种细胞丢失与入院第一天急性发作期间测量的角膜厚度增加显著相关。目前检查时,患眼和未患眼的中央角膜平均厚度相同。然而,发现既往发作眼的眼压有很大差异。如果受试者两眼间眼压差异与两眼间角膜厚度差异相关,则出现显著的负相关。得出结论:眼压对角膜水化有双重作用:如果内皮完整,眼压会降低角膜厚度,而只有在内皮急性受损时才会出现角膜厚度增加。