ferrous-citrate and Brain-Ischemia

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.

Topics: Animals; Brain; Brain Ischemia; Citric Acid; Ditiocarb; Drug Stability; Electron Spin Resonance Spectroscopy; Ferrous Compounds; Iron; Male; Nitric Oxide; Rats; Rats, Sprague-Dawley; Reperfusion