Endothelial-neutrophil interactions during ischemia and reperfusion injury: basic mechanisms of hyperbaric oxygen

Neurol Res. 2007 Mar;29(2):127-31. doi: 10.1179/016164107X174147.


Ischemia/reperfusion injury plays a central role in the development of tissue injury during multiple central nervous system diseases including acute stroke. Neutrophil adhesion to the endothelium indicates a major component of ischemia/reperfusion pathophysiology, and may be a target for therapeutic intervention. Hyperbaric oxygen has been documented to reduce ischemia/reperfusion injury in a number of different experimental models and in a single human randomized clinical trial. One mechanism responsible for the beneficial effect of hyperbaric oxygen in treatment of ischemia/reperfusion injury involves suppression of neutrophil-endothelial adhesion. This review intends to describe the current basic mechanisms responsible for hyperbaric oxygen-mediated inhibition of neutrophil-endothelial interactions following ischemia/reperfusion injury.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Cell Adhesion / physiology
  • Chemotaxis, Leukocyte / physiology*
  • Endothelial Cells / physiology*
  • Humans
  • Hyperbaric Oxygenation / standards*
  • Hypoxia-Ischemia, Brain / immunology
  • Hypoxia-Ischemia, Brain / physiopathology
  • Hypoxia-Ischemia, Brain / therapy*
  • Microcirculation / physiopathology
  • Neutrophils / physiology*
  • Nitric Oxide / metabolism
  • Reperfusion Injury / immunology
  • Reperfusion Injury / physiopathology
  • Reperfusion Injury / therapy*


  • Nitric Oxide