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

Possible involvement of endothelin-1 and nitric oxide in the pathogenesis of proliferative diabetic retinopathy
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DOI:
10.1097/00006982-200112000-00013
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发表时间:
2001-01-01
影响因子:
3.3
通讯作者:
Ikeda, T
Ikeda, T
中科院分区:
医学2区
文献类型:
--
作者:
Oku, H;Kida, T;Ikeda, T

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背景:实验性糖尿病动物视网膜中内皮素-1(ET-1)和一氧化氮(NO)的过度产生。为探讨内皮素-1(ET-1)和一氧化氮(NO)在糖尿病视网膜病变(DR)发病中的作用,作者检测了增生性糖尿病视网膜病变(PDR)患者玻璃体中ET-1和NO的含量(ET-1,n = 12; NO,n = 12)和作为对照的黄斑裂孔患者(ET-1,n = 10; NO,n = 10)。结果:PDR患者玻璃体中内皮素-1水平(平均值± SE)为21.5 ± 1.7 pg/mL,黄斑裂孔患者玻璃体中内皮素-1水平(平均值± SE)为16.7 ± 0.7 pg/mL。PDR患者和对照组之间存在显著差异(P = 0.009,Mann-Whitney)。硝酸盐(NO3)在PDR患者中为49.8 ± 5.0 mumol/L,在黄斑裂孔患者中为24.2 ± 2.8 mumol/L,在PDR患者中也显著升高(P = 0.004,Mann-Whitney),而在本研究中未检测到亚硝酸盐(NO2)。
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 mumol/L in patients with PDR and 24.2 +/- 2.8 mumol/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.