Diabetic patients with retinopathy show increased retinal venous oxygen saturation

• Published in: Graefe's archive for clinical and experimental ophthalmology 2009-08, Vol.247 (8), p.1025-1030
• Main Authors: Hammer, Martin, Vilser, Walthard, Riemer, Thomas, Mandecka, Aleksandra, Schweitzer, Dietrich, Kühn, Uta, Dawczynski, Jens, Liemt, Fanny, Strobel, Jürgen
• Format: Article
• Language: English
• Subjects: Aged; Arterioles - physiology; Blood Flow Velocity; Diabetes Mellitus, Type 2 - blood; Diabetic Retinopathy - blood; Humans; Medicine; Medicine & Public Health; Middle Aged; Ophthalmology; Oximetry; Oxygen - blood; Oxygen Consumption; Regional Blood Flow; Retinal Artery - physiology; Retinal Disorders; Retinal Vein - physiology; Venules - physiology
• ISSN: 0721-832X; 1435-702X
• DOI: 10.1007/s00417-009-1078-6

Background Longstanding diabetes mellitus results in a disturbed microcirculation. A new imaging oximeter was used to investigate the effect of this disturbance on retinal vessel oxygen saturation. Methods The haemoglobin oxygen saturation was measured in the retinal arterioles and venules of 41 diabetic patients (65 ± 12.3 years) with mild non-proliferative through proliferative diabetic retinopathy (DR). Twelve individuals (61.3 ± 6.2 years, mean ± standard deviation) without systemic or ocular disease were investigated as controls. Measurements were taken by an imaging oximeter (oxygen module by Imedos GmbH, Jena). This technique is based on the proportionality of the oxygen saturation and ratio of the optical density of the vessel at two wavelengths (548 nm and 610 nm). Results Whereas there were no significant differences in the arterial oxygen saturation between controls and diabetic retinopathy at any stage, the venous oxygen saturation increased in diabetic patients with the severity of the retinopathy: controls 63 ± 5%, mild non-proliferative DR 69 ± 7%, moderate non-proliferative DR 70 ± 5%, severe non-proliferative DR, 75 ± 5%, and proliferative DR 75 ± 8%. Conclusions The increase of retinal vessel oxygen saturation in diabetic retinopathy points to a diabetic microvascular alteration. This may be due to occlusions and obliterations in the capillary bead and the formation of arterio-venous shunt vessels. On the other hand, hyperglycaemia-induced endothelial dysfunction, with subsequent suppression of the endothelial NO-synthase and disturbance of the vascular auto-regulation, may contribute to retinal tissue hypoxia.