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Lissa Padnick-Silver, PhD; Robert A. Linsenmeier, PhD

Arch Ophthalmol. 2005;123:1684-1690.

Objective  To examine the effects of acute hypoxemia and hyperglycemia on retinal pH to understand hyperglycemia-induced changes in the normal intact cat retina.

Methods  Spatial profiles of extracellular hydrogen ion (H⁺) concentration were obtained from the cat retina, in vivo, using pH-sensitive microelectrodes during normoxia (arterial partial pressure of oxygen [PaO₂] = 114.5 ± 7.9 mm Hg), normoglycemia (plasma glucose concentration, 117 ± 19 mg/dL), acute hypoxemia (PaO₂ = 29.5 ± 2.2 mm Hg), and acute hyperglycemia (plasma glucose concentration, 303 ± 67 mg/dL). An H⁺ diffusion model was fitted to the outer retinal data to quantify photoreceptor H⁺ production. The inner retinal pH was also examined.

Results  Hypoxemia induced a mean acute panretinal acidification of 0.16 pH units that originated from a 2.55-fold increase in net photoreceptor H⁺ production. Hyperglycemia induced an acute panretinal acidification of 0.12 pH units; however, photoreceptor H⁺ production levels remained unchanged. Retinal pH changes followed the course of arterial PaO₂ and blood glucose changes.

Conclusions  The increase in photoreceptor H⁺ production during hypoxemia confirms the importance of glycolysis in the retina. Hyperglycemia-induced pH changes resulted from either increased inner retinal H⁺ production or decreased H⁺ clearance/neutralization.

Clinical Relevance  The hyperglcemia-induced acidification that originates in the inner retina suggests that retinal acidosis may contribute to the development of diabetic retinal disease.

Author Affiliations: Departments of Biomedical Engineering (Drs Padnick-Silver and Linsenmeier) and Neurobiology and Physiology (Dr Linsenmeier), and the Institute for Neuroscience (Dr Linsenmeier), Northwestern University, Evanston, Ill. Dr Padnick-Silver is currently at the Division of Ophthalmology, Evanston Northwestern Healthcare, Glenview, Ill.

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