Abstract
Lung ischemia-reperfusion (IR) injury is one of the most important complications following lung transplant and cardiopulmonary bypass. The pulmonary dysfunction following lung IR has been well documented. Recent studies have shown that ischemia and reperfusion of the lung may each play significant yet differing roles in inducing lung injury. The mechanisms of injury involving neutrophil activation, and the release of numerous inflammatory mediators and oxygen radicals also contributes to lung cellular injury, pneumocyte necrosis, and apoptosis. We herein review the current understanding of the underlying mechanism involved in lung IR injury. The biomolecular mechanisms and interactions which lead to the inflammatory response, pneumocyte necrosis, and apoptosis following lung IR therefore warrant further investigation.
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