Susceptibility of Streptozotocin-Induced Diabetic Rat Retinal Function and Ocular Blood Flow to Acute Intraocular Pressure Challenge
AuthorWong, Vickie H. Y.; Vingrys, Algis J.; Jobling, Andrew I.; Bui, Bang V.
Source TitleINVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
PublisherASSOC RESEARCH VISION OPHTHALMOLOGY INC
University of Melbourne Author/sWong, Vickie; Vingrys, Algis; Jobling, Andrew; Bui, Bang; Cole, Barry
AffiliationOptometry and Vision Sciences
Document TypeJournal Article
Access StatusThis item is currently not available from this repository
NHMRC Grant codeNHMRC/566570
Fulltext embargoed for: 6 months post date of publication
PURPOSE. To consider the hypothesis that streptozotocin (STZ)-induced hyperglycemia renders rat retinal function and ocular blood flow more susceptible to acute IOP challenge.METHODS. Retinal function (electroretinogram [ERG]) was measured during acute IOP challenge (10-100 mm Hg, increments of 5 mm Hg, 3 minutes per step, vitreal cannulation) in adult Long-Evans rats (6 weeks old; citrate: n = 6, STZ: n = 10) 4 weeks after citrate buffer or STZ (65 mg/kg, blood glucose > 15 mM) injection. At each IOP, dim and bright flash (-4.56, -1.72 log cd.s.m(-2)) ERG responses were recorded to measure inner retinal and ON-bipolar cell function, respectively. Ocular blood flow (laser Doppler flowmetry; citrate: n = 6, STZ: n = 10) was also measured during acute IOP challenge. Retinas were isolated for quantitative PCR analysis of nitric oxide synthase mRNA expression (endothelial, eNos; inducible, iNos; neuronal, nNos).RESULTS. STZ-induced diabetes increased the susceptibility of inner retinal (IOP at 50% response, 60.1, CI: 57.0-62.0 mm Hg versus citrate: 67.5, CI: 62.1-72.4 mm Hg) and ON-bipolar cell function (STZ: 60.3, CI: 58.0-62.8 mm Hg versus citrate: 65.1, CI: 61.9-68.6 mm Hg) and ocular blood flow (43.9, CI: 40.8-46.8 versus citrate: 53.4, CI: 50.7-56.1 mm Hg) to IOP challenge. Citrate eyes showed elevated eNos mRNA (+49.7%) after IOP stress, an effect not found in STZ-diabetic eyes (-5.7%, P < 0.03). No difference was observed for iNos or nNos (P > 0.05) following IOP elevation.CONCLUSIONS. STZ-induced diabetes increased functional susceptibility during acute IOP challenge. This functional vulnerability is associated with a reduced capacity for diabetic eyes to upregulate eNos expression and to autoregulate blood flow in response to stress. (Invest Ophthalmol Vis Sci. 2013; 54: 2133-2141) DOI: 10.1167/iovs.13-11595
KeywordsNITRIC-OXIDE SYNTHASE; ENDOTHELIAL GROWTH-FACTOR; NEURAL APOPTOSIS; OPTIC NEUROPATHY; GLIAL-CELLS; B-WAVE; RETINOPATHY; ELECTRORETINOGRAM; DYSFUNCTION; MODEL; NITRIC-OXIDE SYNTHASE; ENDOTHELIAL GROWTH-FACTOR; NEURAL APOPTOSIS; OPTIC NEUROPATHY; GLIAL-CELLS; B-WAVE; RETINOPATHY; ELECTRORETINOGRAM; DYSFUNCTION; MODEL
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