The activities and distributions of succinate dehydrogenase(SDH),malic dehydrogenase(MDH),lactic dehydrogenase(LDH),acid phosphatase(ACP) and alkaline phosphatase(AKP) in retinal vessels were studied and observed with enzymatic histochemical techniques. The retinal vessels showed a b LDH activity, moderate SDH and MDH activity. The dehydrogenase activity described above was evenly and equally distributed in the microvasculature between arterioles and venules, and was the best in arteries. AKP showed predominant activity in the endothelial cells of capillaries and arterioles which were stained bly. No activity for ACP observed in the retinal vessels. The observations above indicate that the retinal vessels are metabolically active and have a great capacity for glycolysis. （Chin J Ocul Fundus Dis,1992,8:6-9）
目的 探讨视网膜微血管直径与2型糖尿病(DM2)并发症糖尿病视网膜病变(DR)的关系。 方法 选取2009年1月-11月住院确诊DM2患者200例，根据眼底彩色照相结果将患者分为DR组和NDR组，测量视网膜血管直径、测定生化指标及血压，用非条件Logistic回归分析糖尿病视网膜病变发生的危险因素。 结果 V1扩张10 μm时，DM2患者并发DR危险性增加(OR 1.75，95% CI 1.14～3.04，Plt;0.05)；空腹血糖水平增加1 mmol/L，DM2患者并发DR的危险性增加(OR 1.87，95% CI 1.43～2.81，Plt;0.05)； 糖化血红蛋白增加1个单位，DM2患者并发DR的危险性增加(OR 1.08，95% CI 1.02～1.13，Plt;0.05)；DM病程增加1年，DM2患者并发DR的危险性增加(OR 1.41，95% CI 1.18～1.70，Plt;0.05)。 结论 在DM2患者中，视网膜静脉直径大小、空腹血糖水平、糖化血红蛋白水平、糖尿病病程是DR发生的危险因素。
ObjectiveTo observe the effect of interleukin-8 (IL-8) on the adhesion and migration of retinal vascular endothelial cells (RCEC). MethodsA cell experiment. Human RCEC (hRCEC) was divided into normal control group (N group), advanced glycation end product (AGE) treatment group (AGE group), and AGE-induced combined IL-8 antagonist SB225002 treatment group (AGE+SB group). The effect of AGE on IL-8 expression in hRCEC was observed by Western blot. The effect of SB225002 on hRCEC migration was observed by cell scratch assay. The effects of SB225002 on leukocyte adhesion and reactive oxygen species (ROS) on hRCEC were detected by flow cytometry. Student-t test was performed between the two groups. One-way analysis of variance was performed among the three groups. ResultsCompared with group N, the expression level of IL-8 in cells of AGE group was significantly increased, with statistical significance (t=25.661, P＜0.001). Compared with N group and AGE+SB group, cell mobility in AGE group was significantly increased (F=29.776), leukocyte adhesion number was significantly increased (F=38.159, 38.556), ROS expression level was significantly increased (F=22.336), and the differences were statistically significant (P＜0.05). ConclusionIL-8 antagonist SB225002 may down-regulate hRCEC adhesion and migration by inhibiting ROS expression.
Objective To observe the expression of p53, bcl-2 genes, vascular endothelial cell growth factor（VEGF）, basic fibroblast growth factor（bFGF）, insulin-like growth factor-I （IGF-I）, and the receptors of these factors of retinal vascular endothelial cells (VECs) of 1- to 20-week diabetic rats, and the relationship between the expressions and cell cycle arrest.Methods Retinal sections of diabetic rats induced by alloxan were immunohistochemically stained and observed by light microscopy (LM) and electron microscopy (EM). Dot blotting and Western blotting were used to determine the expression of mRNA, proteins of p53 and bcl-2. Results Under LM, immunohistochemical positive expression of p53 and bcl-2 were found on the vessels of ganglion cell layer and inner nuclear layer of retinae of 8- to 20-week diabetic rats; under EM, these substances were observed depositing in VECs. The retinal VECs also expressed VEGF, bFGF, IGF-I and their receptors. There was no positive expression of other cell types in these retinae, all cell types of retinae in control group, or all cells of retinae of diabetic rats with the course of disease of 1 to 6 weeks. The result of dot blotting revealed that retinal tissue of 20-week diabetic rat expressed p53 and bcl-2 mRNA, and the result of Western blotting revealed that they also expressed p53 and bcl-2 proteins. But retinal tissues of control group did not. Positive expression of bax was not found in the retinae in control group or 1- to 20-week diabetic rats. Conclusion p53, bcl-2 may introduce cell cycle arrest of VECs of retinae in 8- to 20-week diabetic rats. High glucose might stimulate the expression of VEGF, bFGF, IGF-I and their receptors, and the growth factors may keep VECs surviving by self-secretion. (Chin J Ocul Fundus Dis，2003，19：29-33)
ObjectiveTo measure and analyze the oxygen saturation and retinal blood vessel diameter in the eyes of patients with convalescence Vogt-Koyanagi-Harada (VKH) syndrome. MethodsIn this cross-sectional study, 28 eyes of 14 patients with convalescence VKH syndrome (VKH group) and 20 eyes of 10 healthy subjects (control group) were enrolled. The oxygen saturation and retinal blood vessel diameter were detected by spectrophotometric oximetry unit. Retinal images were collected using filters with wavelengths of 570 nm and 600 nm in the darkroom by the same technologist and then the fused image was obtained. The oxygen saturation of retinal vessels was marked in different colors. The measurement was repeated 2-3 times for each patient, then take an average. A top-quality image in each eye was selected to detect the oxygen saturation and diameter of retinal vessel which located in 1.5-3.0 disc diameter from the optic disc. Image analysis and data acquisition were completed by another technologist. ResultsRetinal venous oxygen saturation was (54.34±8.05)% in the VKH group and (60.07±7.91)% in the control group. The former was lower than the latter, the difference was significant (t=2.443, P=0.017). The mean diameter of retinal arteries was (102.8±18.1) μm in the VKH group and (112.9±19.8) μm in the control group. The former was smaller than the latter, the difference was significant (t=2.406, P=0.018). There was no significant difference of the mean diameter of retinal veins, oxygen saturation of retinal arteries and the arterial-venous difference between two groups (t=-0.330, 0.804, -0.631; P=0.743, 0.403, 0.536). ConclusionsRetinal venous oxygen saturation and the mean diameter of retinal arteries are significantly decreased in patients with VKH syndrome. There is no significant difference of diameter of retinal veins, oxygen saturation of retinal arteries and the arterial-venous difference between VKH syndrome patients and healthy subjects.