Contribution of inflammation to reperfusion injury

Interrupting the flow of blood to an organ for even a relatively brief period disrupts multiple essential vascular homeostatic mechanisms. This results in the cardinal manifestations of reperfusion injury, which, at the tissue level, are comprised of leukocyte infiltration, thrombosis, edema, and vasoconstriction. Molecular mechanisms that are particularly relevant to postischemic inflammation and reperfusion injury include induction of adhesion receptor expression at the endothelial surface, alterations in the procoagulant/anticoagulant balance to promote accumulation of intravascular thrombus, oxidant stress that directly injures cells and indirectly promotes inflammatory upregulation, loss of protective second messenger cyclic nucleotide systems, and activation of the complement cascade that causes vascular injury as well as collateral damage to innocent bystander cells with the reperfused tissue. Understanding the inflammatory mechanisms that participate in reperfusion injury may lead to reperfusion therapies designed to improve postischemic organ function.