Corneal endothelial changes under induced intraocular pressure elevation: a scanning and transmission electron microscopic study in rabbits

• Published in: British journal of ophthalmology 1980-03, Vol.64 (3), p.164-169
• Main Authors: Melamed, S, Ben-Sira, I, Ben-Shaul, Y
• Format: Article
• Language: English
• Subjects: Albinism - pathology; Animals; Cornea - ultrastructure; Corneal Diseases - pathology; Corneal Opacity - pathology; Edema - pathology; Endothelium - ultrastructure; Intraocular Pressure; Microscopy, Electron; Rabbits
• ISSN: 0007-1161; 1468-2079
• DOI: 10.1136/bjo.64.3.164

Intraocular pressure was artificially raised to 60--70 mmHg in 7 albino rabbits for periods of 15 minutes to 4 hours. The corneal endothelium of these eyes was studied by transmission and scanning electron microscopy. A correlation between exposure time to elevated IOP, clinical signs observed by slit-lamp examination, and extent of morphological damage is clearly shown. In eyes exposed to high pressure for 15 and 30 minutes corneas remained transparent and only minimal changes could be detected by SEM, which consisted of small areas of cell with unevenness of their surface, occasional cellular ruptures, and diminution of cilia and microvilli. After 1--2 hours of exposure small, solitary corneal opacifications appeared. In these eyes more severe morphological changes affecting larger areas were observed, with additional cellular blebbing, excariocytosis, cellular rupture, disintegration, and disappearance seen in SEM. Thin sections revealed swelling of mitochondria, disorganisation of endoplasmic reticulum, and the existence of myelin bodies. In eyes exposed for 3 and 4 hours to high IOP corneal haziness, implying stromal oedema, appeared. In these eyes the areas affected were larger, the extent of damage being more severe. Many areas were bare of endothelium, surrounded by scattered cellular debris, and showed cells with ballooning surfaces and multiple ruptures. Even in severe cellular damage cellular junctions appeared intact. It is assumed that endothelial cells are more sensitive to IOP elevation than the cellular junctions and that injury to the active pump system due to morphological damage is responsible for the resultant corneal oedema.