Insulin-induced nitric oxide production and high glucose in microvessels of rat retina

评估胰岛素诱导的视网膜微血管一氧化氮（NO）的产生。在不同浓度的葡萄糖和不加胰岛素的情况下培养视网膜微血管。采用激光扫描共聚焦显微镜延时记录DAF荧光强度，半定量测定视网膜微血管NO生成的变化。此外，采用台盼蓝法测定各组周细胞的活力。在5.5 mM葡萄糖中，微血管暴露于胰岛素中，荧光强度显著增加，而在20 mM葡萄糖中，微血管暴露于胰岛素中，胰岛素诱导的NO产生明显受到抑制。胰岛素增加一氧化氮的产生，并可能促进视网膜的微循环。然而，这种no介导的胰岛素作用在高糖条件下被抑制。这些结果可能解释了糖尿病患者视网膜循环受损的原因。

Insulin-induced nitric oxide (NO) production in retinal microvessels was evaluated. The retinal microvessels were incubated in different concentration of glucose with or without addition of insulin. Changes of NO production in the retinal microvessels were semiquantitatively determined by the time-lapse recording offluorescent intensity of DAF using a laser scanning confocal microscope. In addition, cell viability of pericyte in each condition was assayed by trypan blue exclusion. Exposure of microvessels to insulin in 5.5 mM glucose, the fluorescent intensity was significantly increased, while the insulin-induced NO production was significantly suppressed when vessels were incubated in 20 mM glucose. Insulin increased production of NO and may contribute to the microcirculation of retina. However, this NO-mediated action of insulin is suppressed under high glucose condition. These results may account for impairment of retinal circulation under diabetic conditions.