TY - JOUR
T1 - Effect of hypoxemia and hyperglycemia on pH in the intact cat retina
AU - Padnick-Silver, Lissa
AU - Linsenmeier, Robert A.
PY - 2005/12
Y1 - 2005/12
N2 - 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 [PaO 2]=114.5±7.9 mm Hg), normoglycemia (plasma glucose concentration, 117±19 mg/dL), acute hypoxemia (PaO 2=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 PaO 2 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.
AB - 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 [PaO 2]=114.5±7.9 mm Hg), normoglycemia (plasma glucose concentration, 117±19 mg/dL), acute hypoxemia (PaO 2=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 PaO 2 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.
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U2 - 10.1001/archopht.123.12.1684
DO - 10.1001/archopht.123.12.1684
M3 - Article
C2 - 16344440
AN - SCOPUS:28944453758
SN - 0003-9950
VL - 123
SP - 1684
EP - 1690
JO - Archives of ophthalmology
JF - Archives of ophthalmology
IS - 12
ER -