Contribution of inflammation to reperfusion injury

Interrupting the flow of blood to an organ for even a relatively brief peri od disrupts multiple essential vascular homeostatic mechanisms. This result s in the cardinal manifestations of reperfusion injury, which, at the tissu e level, are comprised of leukocyte infiltration, thrombosis, edema, and va soconstriction. Molecular mechanisms that are particularly relevant to post ischemic inflammation and reperfusion injury include induction of adhesion receptor expression at the endothelial surface, alterations in the procoagu lant/anticoagulant balance to promote accumulation of intravascular thrombu s, oxidant stress that directly injures cells and indirectly promotes infla mmatory upregulation, loss of protective second messenger cyclic nucleotide systems, and activation of the complement cascade that causes vascular inj ury as well as collateral damage to innocent bystander cells with the reper fused tissue. Understanding the inflammatory mechanisms that participate in reperfusion injury may lead to reperfusion therapies designed to improve p ostischemic organ function.