一氧化氮与视网膜缺血-再灌注损伤

一氧化氮（NO）在视网膜缺血-再灌注损伤中占重要地位。视网膜缺血-再灌注时,一氧化氮合成酶（NOS）被多种炎性介质和细胞因子激活,使NO大量生成。NO是一种活性很强的自由基,具有广泛的生物学活性。在缺血-再灌注早期,少量NO可降低缺血缺氧对视网膜的损伤程度;晚期过多的NO可通过多种途径对视网膜造成损害。就目前有关NO在视网膜缺血-再灌注损伤中的研究进展进行综述。

Nitric oxide and retinal ischemia-reperfusion injury

Nitric oxide （NO） plays an important role in retinal ischemia-reperfusion injury. Nitric oxide synthase is activated by many kinds of mediators of inflammation and cytokines and therefore produce generous NO under the retinal ischemia-reperfusion condition. NO is a free radical with widely biologic activities. In the earlier period of retinal ischemia- reperfusion injury,a little of NO contents can decline the injury degree of retina by ischemic and hypoxia down. However,at the advanced stage of retinal ischemia-reperfusion injury, a great amount of NO damage retina via multiple physiological and pathological approaches. To identify the injury mechanism of NO to retina and control its excessive production is very critical for preventing and treating ischemia-reperfusion injury of retina. The research advance in effects of NO on ischemia-reperfusion injury of retina is reviewed.