Andreas Ebneter, Glyn Chidlow, John Wood, Robert Casson
The Ocular Hypertension Treatment Study (OHTS) reported that diabetes protected against the conversion of ocular hypertension (OHT) to glauco-matous optic neuropathy (GON). Hyperglycemia is neuroprotective in rodent models of acute retinal isch-emia and chronic retinal hypoperfusion. The aim of the current work was to investigate the effect of short-term hyperglycemia on optic nerve damage in a rat model of experimental glaucoma.
Experimental GON was induced in a group of normoglycemic (n = 26) and a group of hypergly-cemic (n = 26) Sprague-Dawley rats by layering the trabecular meshwork using a standard protocol. After two weeks of elevated intraocular pressure, rats were killed by transcardial perfusion.Axonal loss was graded semi-quantitatively on trans-verse sections of the optic nerve. Longitudinal sections were immunohistochemically stained for glial markers. The histological/immunohistochemical outcomes were compared using unpaired, non-parametric statistics.
The degree of axonal loss following 2 weeks of experimental glaucoma was significantly lower in the hyperglycemic group of rats compared to the nor-moglycemic group. Axonal loss was reduced by 54%.
Underlying hyperglycemia appeared to be protective in this rat model of experimental GON after 2 weeks of OHT. Possible explanations for this effect are the attenuation of malperfusion induced energy failure by increasing the substrate for glycolysis or a shift in metabolism resulting in reduction of ROS-induced apoptosis.
GLISTENINGS IN INTRAOCULAR LENSES IN AUSTRALIA AND NEW ZEALAND- A COLLABORATIVE SURGICAL QUALITY AUDIT OVER THE 24 MONTH PERIOD UP TO FEBRUARY 2017. FINDINGS OF THIS AUDIT OF LENSES IMPLANTED BETWEEN 1995 AND 2016, HIGHLIGHT THE ONGOING PRESENCE AND SEVERITY OF VACUOLES EVEN IN THE MOST RECENTLY IMPLANTED LENSES.