一氧化氮及一氧化氮合酶在脑缺血损伤中的作用

一氧化氮(NO)在脑内具有重要的血管和神经作用.生物体内L-精氨酸与O2在一氧化氮合酶(NOS)作用下生成NO.脑缺血发生后即有短暂的NO增高,主要由神经元的nNOS及血管内皮的eNOS介导,24 h后出现延迟性的更为明显的NO升高,这可能源于nNOS及iNOS的缓慢上调.不同来源的NO在脑缺血损伤中所起的作用是不同的.NO对神经元的损伤可能与其介导兴奋性氨基酸的作用及其自身的氧化还原状态有关.NO的半衰期很短,大量研究通过对NOS、L-氨酸及特异性酶抑制剂的了解,熟悉不同来源的NO的作用,有助于脑缺血的临床治疗及愈后.

Investigation of NO and NOS in cerebral ischemia

NO plays an important role in the pathogenesis of neural injury during cerebral ischemia. Nitric Oxide synthase(NOS) converts L arginene into NO,but NO generation from three distinct forms of NOS can have different roles in the process of ischemia injury.NO produced by eNOS appears to play a protective roleduring and after cerebual ischemia .In contrast,high concentration NO produced by nNOS and iNOS may aggravate the metabolic state of the ischemic tissue,thereby contributing to brain injury.The half life of NO is so short that many studies of NO rely on NOS, L Arg and NOS inhibitor.NO donor and NOS inhibitors have been becoming a new subject in clinic and basic researches for the protection of focal cerebral ischemic injury.