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Effect of subconjunctival glucose on retinal ganglion cell survival in experimental retinal ischaemia and contrast sensitivity in human glaucoma
Author(s) -
Shibeeb O'Sam,
Chidlow Glyn,
Han Guoge,
Wood John PM,
Casson Robert J
Publication year - 2015
Publication title -
clinical and experimental ophthalmology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.3
H-Index - 74
eISSN - 1442-9071
pISSN - 1442-6404
DOI - 10.1111/ceo.12581
Subject(s) - medicine , retinal , ophthalmology , glaucoma , retinal ganglion cell , saline , retina , optic nerve , ocular hypertension , anesthesia , biology , neuroscience
Purpose This study aims to evaluate the effect of subconjunctival glucose on the retinal ganglion cells ( RGCs ) in experimental retinal ischaemia and contrast sensitivity in humans with primary open‐angle glaucoma ( POAG ). Methods First, we measured the intravitreal concentration of glucose at various time points after a subconjunctival injection of 100 μl of 50% glucose to S prague‐ D awley rats. Next, treatment and control groups received 50% subconjunctival glucose and iso‐osmotic (8%) saline, respectively, 1 h prior to a unilateral ischaemic retinal injury; 7 days later, the damage profiles were compared using RGC and axon counts. Subsequently, we conducted a double‐blind, crossover, pilot clinical study in seven eyes of five pseudophakic subjects with severe POAG . Subjects received either 0.3 mL of 50% glucose subconjunctivally or iso‐osmotic (8%) saline, then vice versa after a 2–3 week ‘wash‐out’ period; change in contrast sensitivity from baseline was the primary outcome. Results Subconjunctival glucose preserved approximately 60% of Brn3a‐positive RGCs in all retinal zones compared with an 80% loss in control retinas, and rescued approximately 40% of the axonal loss. In the human trial, the contrast sensitivity at 12 cycles/degree was 0.24 log units greater than baseline (95% confidence interval 0.12–0.36; P < 0.001). Conclusions Subconjunctival glucose partially protects RGC somata and axons against an ischaemic insult and temporarily recovers contrast sensitivity in patients with severe POAG . Although an unlikely therapeutic strategy for POAG , the findings motivate further bioenergetic‐based research in glaucoma and other optic nerve and retinal diseases, where energy failure may be part of the pathogenesis.