The obstacle of intestinal ischemia/reperfusion (IIR) is not necessarily limited to the intestine itself, but involves in the distant tissue severe destruction because of reperfused toxin blood. It is known that IIR is an important inciting event in the pathogenesis of multiple organ disfunction syndrome (MODS) and systemic inflammatory response syndrome (SIRS), which is the leading cause of death in critically ill patients. Up to now, IIR is still an interference for intestinal transplantation. There is a high mortality in intestinal ishemia disease.The mechanism of liver and lung injury induced by IIR is complex. Traditionally, proinflammatory cytokines and chemokines have been considered to exert their effects via a direct toxic action on target cells, intercellular adhesion molecule-1 (ICAM-1) and neutrophil infiltration play an important role in liver and lung injury induced by IIR. However, recent studies showed a role for these proinflammatory mediators in gene induction. Nuclear factor kappa B (NFκB) up-regulated most of these mediators, but it is not known if and how NFκB is activated and ICAM-1 expressed in liver and lung injury induced by intestinal ischemia.
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