Attenuation of free radical generation during reversible focal cerebral ischemia with the nitric oxide inhibitor, L-NAME (L-N(G)-nitro-L-arginine methyl ester).
Attenuation of free radical generation during reversible focal cerebral ischemia with the nitric oxide inhibitor, L-NAME (L-N(G)-nitro-L-arginine methyl ester).
复制标题
使用一氧化氮抑制剂 L-NAME（L-N(G)-硝基-L-精氨酸甲酯）可减少可逆性局灶性脑缺血期间自由基的产生。
DOI：
10.1016/s0006-8993(00)02088-6
复制
发表时间：
2000
期刊：
影响因子：
2.9
通讯作者：
Kwan,A
中科院分区：
文献类型：
--
作者：
Solenski,NJ;Kwan,A
研究了氧自由基在可逆性局灶性脑缺血中产生的作用及其与一氧化氮介导机制的关系。在这项研究中，将左额叶皮层微透析探针放置在先前定义的缺血半暗带区，并在一氧化氮合酶（NOS）抑制剂l-NAME存在或不存在的情况下灌注水杨酸盐/CSF溶液。然后对大鼠进行短暂性左半球局灶性脑缺血。在基线和缺血/再灌注阶段收集透析液，采用HPLC电化学检测水杨酸羟基化产物。在缺血/再灌注期间，观察到半暗区自由基加合物形成显著升高。这种升高在再灌注期被l-NAME显著减弱。脑缺血/再灌注时半暗区自由基加合物形成的升高可能部分由nos依赖机制介导。
The role of oxygen free radical generation during reversible focal cerebral ischemia and its relationship to nitric oxide mediated mechanisms were examined. In this study, a left frontal cortex microdialysis probe was placed into the previously defined ischemic penumbra region and perfused with a salicylate/CSF solution in the presence or absence of the nitric oxide synthase (NOS) inhibitor l-NAME. Rats were then subjected to transient left hemisphere focal cerebral ischemia. Dialysate was collected at baseline and during the ischemic/reperfusion phase, and the hydroxylation products of salicylate were measured by HPLC with electrochemical detection. A significant elevation of free radical adduct formation was observed in the penumbra region during ischemia/reperfusion. This elevation was significantly attenuated by l-NAME during the reperfusion phase. Elevation of free radical adduct formation within the penumbra region during cerebral ischemia/reperfusion may be mediated in part by NOS-dependent mechanisms.