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Hyperbaric oxygenation alleviates MCAO-induced brain injury and reduces hydroxyl radical formation and glutamate release.

Abstract
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.
AuthorsZhong-jin Yang, Yan Xie, Geraldo M Bosco, Chung Chen, Enrico M Camporesi
JournalEuropean journal of applied physiology (Eur J Appl Physiol) Vol. 108 Issue 3 Pg. 513-22 (Feb 2010) ISSN: 1439-6327 [Electronic] Germany
PMID19851780 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Gentisates
  • Glutamates
  • Hydroxybenzoates
  • Hydroxyl Radical
  • 2,3-dihydroxybenzoic acid
  • 2,5-dihydroxybenzoic acid
Topics
  • Animals
  • Blood Pressure (physiology)
  • Brain (metabolism)
  • Brain Injuries (etiology, metabolism, therapy)
  • Gentisates (metabolism)
  • Glutamates (metabolism)
  • Hydroxybenzoates (metabolism)
  • Hydroxyl Radical (metabolism)
  • Hyperbaric Oxygenation
  • Infarction, Middle Cerebral Artery (complications)
  • Male
  • Models, Animal
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury (etiology, metabolism, therapy)

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