Sato S, Tominaga T, Ohnishi T, Ohnishi S T
Philadelphia Biomedical Research Institute, King of Prussia, PA 19406.
Brain Res. 1994 May 30;647(1):91-6. doi: 10.1016/0006-8993(94)91402-8.
The production of nitric oxide (NO) during brain focal ischemia and reperfusion was measured using diethyldithiocarbamate (DETC)/Fe-citrate, NO trapping reagents, and electron paramagnetic resonance spectroscopy. The NO production is potentiated after 5 min of ischemia, and is continued during 60 min of ischemia. During the reperfusion period after 60 min of ischemia, NO was also produced. However, its production during reperfusion was not observed when the ischemia time was less than 15 min. The NO signal during reperfusion after 60 min of ischemia decreased after 15 min of reperfusion. These results suggest that NO production during ischemia is a physiological reaction for increasing cerebral blood flow, while NO production during reperfusion may be related to cellular damage.
使用二乙基二硫代氨基甲酸盐（DETC）/柠檬酸铁、一氧化氮捕获试剂和电子顺磁共振光谱法测量脑局灶性缺血和再灌注期间一氧化氮（NO）的产生。缺血5分钟后一氧化氮的产生增强，并在60分钟的缺血期间持续。在缺血60分钟后的再灌注期，也产生了一氧化氮。然而，当缺血时间小于15分钟时，未观察到再灌注期间一氧化氮的产生。缺血60分钟后再灌注期间的一氧化氮信号在再灌注15分钟后下降。这些结果表明，缺血期间一氧化氮的产生是增加脑血流量的生理反应，而再灌注期间一氧化氮的产生可能与细胞损伤有关。
