The present study examined the effect of hyperbaric
oxygen (HBO) on the formation of
2,3-dihydroxybenzoic acid (2,3-DHBA) and
2,5-dihydroxybenzoic acid (2,5-DHBA), the products of
salicylate trapping of
hydroxyl free radicals, and
glutamate release in the striatum during acute
ischemia and reperfusion. Non-HBO rats (n = 8) were subjected to 1-h
ischemia. Study rats (n = 8) were treated with HBO at 2.8 ATA for 1 h during
ischemia. Artificial CSF
solution containing 5 mM
sodium salicylate was perfused at 1 microl/min. Samples were continuously collected at 15 min intervals and the levels of 2,3-DHBA, 2,5-DHBA, and
glutamate were analyzed. The lesion volume was determined by TTC
stain. Occlusion of the middle cerebral artery induced a significant increase in the levels of 2,3-DHBA and 2,5-DHBA. A peak of approximately two and fourfold of baseline levels was reached at 45 min and was maintained at elevated levels during reperfusion. The level of
glutamate increased approximately two times at 30 min during
ischemia, continued to increase, and reached approximately three times baseline level during reperfusion. HBO significantly alleviated
brain injury associated with decreased levels of 2,3-DHBA, 2,5-DHBA and
glutamate. This study suggests that the decreased
glutamate release and the reduced formation of
hydroxyl free radicals might contribute to the
neuroprotective effect of HBO.