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.

Buras, Reenstra, , , , , , , (2007). Endothelial-neutrophil interactions during ischemia and reperfusion injury: basic mechanisms of hyperbaric oxygen. Neurological research, 2007 Mar;29(2):127-31. https://www.ncbi.nlm.nih.gov/pubmed/17439696