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

评价了胰岛素诱导的视网膜微血管中一氧化氮（NO）的产生。将视网膜微血管在不同浓度的葡萄糖中孵育，加入或不加入胰岛素。用激光扫描共聚焦显微镜对视网膜微血管中NO的产生进行半定量测定。此外，通过台盼蓝拒染法测定每种条件下周细胞的细胞活力。将微血管暴露于5.5 mM葡萄糖中的胰岛素，荧光强度显著增加，而当血管在20 mM葡萄糖中孵育时，胰岛素诱导的NO产生被显著抑制。胰岛素可增加NO的生成，并可能对视网膜微循环有一定的促进作用。然而，这种NO介导的胰岛素作用在高糖条件下受到抑制。这些结果可以解释糖尿病条件下视网膜循环的损害。

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.