title: Endothelial-neutrophil interactions during ischemia and reperfusion injury: basic mechanisms of hyperbaric oxygen.
abstract: 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.
authors: Department of Biology and Department of Pharmaceutical Sciences, New England Inflammation and Tissue Protection Institute at Northeastern University, Boston, MA 02115, USA. jburas@mac.com
authors: J A
authors: JA
authors: Buras
authors: W R
authors: WR
authors: Reenstra
mesh_terms: D000818:Animals; D002448:Cell Adhesion / Q000502:physiology; D002634:Chemotaxis, Leukocyte / Q000502:physiology*; D042783:Endothelial Cells / Q000502:physiology*; D006801:Humans; D006931:Hyperbaric Oxygenation / Q000592:standards*; D020925:Hypoxia-Ischemia, Brain / Q000276:immunology / Q000503:physiopathology / Q000628:therapy*; D008833:Microcirculation / Q000503:physiopathology; D009504:Neutrophils / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism; D015427:Reperfusion Injury / Q000276:immunology / Q000503:physiopathology / Q000628:therapy*
chemical_list: D009569:Nitric Oxide