Buras J A, Reenstra W R
Department of Biology and Department of Pharmaceutical Sciences, New England Inflammation and Tissue Protection Institute at Northeastern University, Boston, MA 02115, USA.
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.
缺血/再灌注损伤在包括急性中风在内的多种中枢神经系统疾病的组织损伤发展过程中起着核心作用。中性粒细胞与内皮细胞的黏附是缺血/再灌注病理生理学的一个主要组成部分，可能是治疗干预的靶点。在许多不同的实验模型和一项人体随机临床试验中，均已证明高压氧可减轻缺血/再灌注损伤。高压氧治疗缺血/再灌注损伤产生有益作用的一种机制涉及抑制中性粒细胞与内皮细胞的黏附。本综述旨在描述目前关于高压氧介导缺血/再灌注损伤后中性粒细胞与内皮细胞相互作用受抑制的基本机制。
