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Bruce A. Berkowitz, Yasuki Ito, Timothy S. Kern, Christopher McDonald, Roberta Hawkins; Correction of Early Subnormal Superior Hemiretinal ΔPO2 Predicts Therapeutic Efficacy in Experimental Diabetic Retinopathy. Invest. Ophthalmol. Vis. Sci. 2001;42(12):2964-2969.
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© ARVO (1962-2015); The Authors (2016-present)
purpose. To test the hypothesis that regional retinal oxygenation responses to a
hyperoxic inhalation challenge are associated with reported retinopathy
outcomes after different therapies in rat models of diabetic
methods. Six groups of rats were maintained for 3 months: controls (n= 8), untreated diabetic (n = 8), aminoguanidine
(AMG)-treated diabetic (2.5 g/kg of diet; n = 6),
untreated galactosemic (n = 7), AMG-treated galactosemic
(n = 10), and WAY-509–treated (25 mg/kg body weight per
day) galactosemic (n = 7). After 3 months, the change in
oxygen tension was measured noninvasively from the superior to the
inferior ora serrata, using a novel functional magnetic resonance
imaging (fMRI) technique and a carbogen (a gas mixture of 5% carbon
dioxide and 95% oxygen that has been used clinically, instead of 100%
oxygen, to minimize the vasoconstrictive effects of pure O2 on retinal blood flow and oxygenation) inhalation challenge. Retinal
morphometric measurements were also obtained.
results. Retinal lesions (acellular capillaries and pericyte ghosts) were not
significantly (P > 0.05) present at 3 months in
any experimental groups compared with the control group. Superior but
not inferior hemiretinal change in partial pressure of oxygen
(ΔPO2) became significantly subnormal
(P < 0.05) at 3 months of diabetes or
galactosemia. Aminoguanidine, which has been found to inhibit the
development of retinopathy in diabetic but not galactosemic rats,
inhibited the development of a subnormal ΔPO2 in diabetes
but not in galactosemia. WAY-509, which has been reported to inhibit
retinopathy in galactosemic rats, inhibited the ΔPO2 defect in galactosemic rats.
conclusions. An early subnormal superior hemiretinal ΔPO2 after
treatment appears to be a good predictor of the risk of development of
retinopathy, as well as for assessing therapeutic efficacy in
experimental diabetic retinopathy.
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