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Possible involvement of endothelin-1 and nitric oxide in the pathogenesis of proliferative diabetic retinopathy.

机译:内皮素1和一氧化氮可能参与增生性糖尿病视网膜病变的发病机制。

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BACKGROUND: Overproduction of endothelin-1 (ET-1) and nitric oxide (NO) in the retina is demonstrated in experimental diabetic animals. To clarify the possible involvement of ET-1 and NO in the pathogenesis of diabetic retinopathy, the authors examined the vitreous levels of these principal endothelium-derived vasoactive substances in patients with proliferative diabetic retinopathy (PDR). METHODS: Vitreous fluid was taken from patients with PDR (ET-1, n = 12; NO, n = 12) and from patients with macular holes as controls (ET-1, n = 10; NO, n = 10) at vitreous surgery. Endothelin-1 and NO metabolites were measured by radioimmunoassay and high-performance liquid chromatography based on the Griess method, respectively. RESULTS: Endothelin-1 levels (mean +/- SE) were 21.5 +/- 1.7 pg/mL in the vitreous of patients with PDR and 16.7 +/- 0.7 pg/mL in the vitreous of patients with macular hole. There was a significant difference between patients with PDR and controls (P = 0.009, Mann-Whitney). Nitrate (NO3) was 49.8 +/- 5.0 micromol/L in patients with PDR and 24.2 +/- 2.8 micromol/L in patients with macula hole; it was also significantly elevated in patients with PDR (P = 0.004, Mann-Whitney), whereas nitrite (NO2) was not detected in this study. CONCLUSION: These results indicate that ET-1 and NO may be related in the pathogenesis of PDR.
机译:背景:在实验性糖尿病动物中,视网膜中内皮素1(ET-1)和一氧化氮(NO)的过量生产被证明。为了阐明ET-1和NO可能参与糖尿病性视网膜病的发病机制,作者检查了增殖性糖尿病性视网膜病(PDR)患者中这些主要内皮源性血管活性物质的玻璃体水平。方法:玻璃体液取自PDR患者(ET-1,n = 12; NO,n = 12)和黄斑裂孔作为对照(ET-1,n = 10; NO,n = 10)。手术。内皮素-1和NO代谢物分别通过放射免疫分析和基于Griess方法的高效液相色谱法进行测量。结果:PDR患者玻璃体中内皮素1的水平(平均值+/- SE)为21.5 +/- 1.7 pg / mL,黄斑裂孔患者玻璃体中的内皮素1水平为16.7 +/- 0.7 pg / mL。 PDR患者与对照组之间存在显着差异(P = 0.009,Mann-Whitney)。 PDR患者的硝酸盐(NO3)为49.8 +/- 5.0 micromol / L,黄斑裂孔患者的硝酸盐(NO3)为24.2 +/- 2.8 micromol / L。 PDR患者的血红蛋白水平也显着升高(P = 0.004,Mann-Whitney),而本研究中未检测到亚硝酸盐(NO2)。结论:这些结果表明ET-1和NO可能与PDR的发病有关。

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