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。
Objective To investigate the spatial and temporal regulation effect of VEGF on human fetal retinal vascularization and angiogenesis. Methods The posterior segmental retinas from 54 human fetuses of the 9th week to the 40th week were studied by immunohistodhemistry standing for the expressions of VEGF and PCNA. Results 1. The distribution of VEGF espression was spiking and the peaks were during the 9th-13th and around the 26th week. 2. PCNA immunoreactivity was localized in spindle cells and vascular endothelial cells. The expression level was fluctuated during the developmental process. The peaks were during the 9th-13th and around the 21st week. In these periods, the spindle cells kept proliferating and differentiating, and remodelled subsequently to form the inner side retinal vessels. From the 26th or 34th week, the PCNA immununoreactivity is fully expressed in the vascular endothelial cells of the inner and outer margin of inner nuclear layer(INL) and kept to full terms. 3. Significant positive correlation were shown between the content of VEGF in the retina and that of PCNA in spindle cells and vascular endothelial cells(r=0.736,p＜0.01). Conclusion VEGF was positively involved in modulating human fetal retinal vascularization and angiogenesis. (Chin J Ocul Fundus Dis,1999,15:12-15)
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)
Objective To investigate the effect of hypoxia on the exp ression and function of integrin receptor αvβ3 of bovine retinal vascular endotheliocytes. Methods Bovine retinal vascular endotheliocy tes in the culture dishes coated by vitronectin was put into the normal and hypoxemic condition, respectively. Enzyme linked immunosorbent assay and cell adhesion analysis were used to detect the expression and function of integrin receptor αvβ3 in bovine retinal vascular endotheliocytes, respectively. Results Under the condition of hypoxia, the expression of αvβ3 increased gradually, and reached the peak at the 48th hour. The expression of αvβ3 at the 60th and 72nd hour in hypoxia group was higher than that in the normal group. Bovine retinal vascular endotheliocytes absorbed more Vn of extra-cellular matrixes (ECM) after cultured under hypoxemic condition for 24 hours.Conclusion Hypoxia may up-regulate the expression of αvβ3, which promote the adsorbability of endotheliocytes.(Chin J Ocul Fundus Dis，2004，20：360-363)
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.
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）
Objective To investigate the characteristics of fundus photography and fundus fluorescein angiography (FFA) of IRVAN (idiopathic retinal vasculitis, aneurysms, and neuroretinitis) syndrome and Eales disease. Methods The fundus photography and FFA data of 4 cases (8 eyes) with IRVAN syndrome and 43 cases (68 eyes) with Eales disease were retrospectively analyzed. All patients received ophthalmic routine examinations, including visual acuity, intraocular pressure, slit-lamp microscope and indirect ophthalmoscope. All patients had taken fundus photography and FFA for both eyes, except 4 patients of Eales disease who had vitreous hemorrhage in one eye. All 4 cases(1 male/3 female )with IRVAN syndrome were bilateral and aged 1643 years old( mean age 2700plusmn;1293 years old). 43 cases (32 male/11 female) of Eales disease aged 6-59 years old( mean 30.79plusmn;11.46 years old), 29 cases were bilateral and 14 cases were unilateral. Both diseases had retinal vascular whitesheath or white threadlike changes, exudative retinal hemorrhage and vitreous hemorrhage. Results Both arteries and veins of posterior pole of all eyes with IRVAN syndrome were involved and shown multiple retinal macroaneurysms. Other signs of IRVAN syndrome included capillary occlusion and nonperfusion (7/8 eyes, 87.5%),fluorescein leakage and edema of optic disc (5/8 eyes,62.5%), optic atrophy(2/8 eyes,25%), vitreous hemorrhage(1/8 eyes,12.5%), neovascularization of optic disc(2/8 eyes,25%), retinal neovascularization(4/8 eyes,50%) and macular edema(4/8 eyes,50%). The signs of Eales disease included fluorescein leakage of peripheral retinal vein (68/68 eyes, 100%), fluorescein leakage of posterior retinal vein (32/68 eyes, 47.06%), artery involvement (5/68 eyes, 7.35%), peripheral capillary occlusion and nonperfusion (38/68 eyes, 55.88%), fluorescein leakage of optic disc(29/68 eyes, 42.65%), neovascularization of optic disc(4/68 eyes,5.88%), retinal neovascularization(26/68 eyes,38.2%) and macular edema(15/68 eyes,22.06%). Compared IRVAN syndrome with Eales disease, the difference of artery inflammation, vein inflammation, retinal macroaneurysms in posterior area had statistics significance(all P=000,Plt;005), and that of edema of optic disc, retinal vascular nonperfusion area, neovascularization of optic disc, neovascularization elsewhere, and macular edema had no statistics significance(chi;2=0.479，P＞0.05；P=0.131，P＞0.05；chi;2=1.449，P＞0.05；chi;2=0.068，P＞0.05；chi;2=1.676，P＞0.05). Conclusions Both IRVAN syndrome and Eales disease may have vein and artery inflammation in posterior pole of the eye, and may result in neuroretinitis. IRVAN syndrome has much more vein and artery inflammation in posterior pole than Eales disease. Posterior retinal macroaneurysms is the most important sign for the diagnosis and differential diagnosis of IRVAN syndrome and Eales disease.