Diabetic patients with retinopathy show increased retinal venous oxygen saturation
Diabetic patients with retinopathy show increased retinal venous oxygen saturation
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DOI：
10.1007/s00417-009-1078-6
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发表时间：
2009-08-01
影响因子：
2.7
通讯作者：
Strobel, Juergen
中科院分区：
文献类型：
--
作者：
Hammer, Martin;Vilser, Walthard;Strobel, Juergen
长期的糖尿病导致微循环障碍。为探讨糖尿病视网膜病变对视网膜血管血氧饱和度的影响，应用一种新的血氧仪对41例轻度非增殖性至增殖性糖尿病视网膜病变(DR)患者的视网膜小动脉和小静脉血氧饱和度进行了测定。12名无全身或眼部疾病的个体(61.3+/-6.2岁，平均+/-A标准差)作为对照。通过成像血氧仪(Imedos GmbH，Jena的氧气模块)进行测量。这项技术是基于两个波长(548 nm和610 nm)的血氧饱和度和血管光密度的比率。在任何时期，对照组和糖尿病视网膜病变患者的动脉血氧饱和度没有显著差异，但随着视网膜病变的严重程度，糖尿病患者的静脉血氧饱和度增加：对照组63+/-5%，轻度非增殖性DR 69+/-7%，中度非增殖性DR 70+/-5%，重度非增殖性DR，75+/-5%，糖尿病视网膜病变患者视网膜血管血氧饱和度升高，提示糖尿病微血管病变。这可能是由于毛细血管小球闭塞和闭塞以及动静脉分流血管的形成所致。另一方面，高血糖引起的内皮功能障碍，继而导致内皮一氧化氮合酶的抑制和血管自我调节的紊乱，可能是视网膜组织缺氧的原因之一。
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.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 +/- A 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).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%.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.