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1From the Department of Ophthalmology, Henry Ford Health System, Detroit, Michigan; and the 2Department of Anatomy and Cell Biology and the 3Kresge Eye Institute, Wayne State University, Detroit, Michigan.
PURPOSE. To determine whether the human retinal oxygenation response (
PO2) to a hyperoxic provocation is abnormal in patients with type I diabetes.
METHODS. Magnetic resonance imaging (MRI) was used to measure
PO2 during 100% oxygen breathing in patients with type I diabetes who had either no clinically detectable retinopathy (n = 5) or mild to moderate background diabetic retinopathy (BDR; n = 5) and in age-matched healthy control subjects (n = 7).
RESULTS. Both the patients with diabetes and the control subjects exhibited a significant (P < 0.05) increase in the preretinal vitreous signal intensity on changing from room air breathing to oxygen inhalation (i.e., 5 minutes). However, only diabetic patients demonstrated significant (P < 0.05) increases in
PO2 between measurements made at 5 minutes of oxygen inhalation and measurements at longer durations of hyperoxia (15, 25, and 35 minutes). Furthermore,
PO2 was significantly (P < 0.05) greater in patients with diabetes than in control subjects, but there was no significant difference in
PO2 (P > 0.05) between patients with diabetes, with or without retinopathy. Age and
PO2 correlated significantly (P < 0.05) in control subjects but not in patients with diabetes. In control subjects,
PO2 was relatively uniform panretinally, whereas in the diabetic group, changes in oxygenation response were spatially inhomogeneous.
CONCLUSIONS. These results demonstrate, for the first time, that MRI
PO2 detects a significant supernormal retinal oxygenation response in patients with type I diabetes, even before the appearance of retinopathy. This study raises the possibility of using MRI measurements of
PO2 to monitor therapeutic efficacy in human trials.
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