ABSTRACT
The activated neutrophils mediate the vascular injury that is associated with reperfusion. This chapter summarizes the evidence that provides the basis for the xanthine oxidase/neutrophil hypothesis of reperfusion injury. D. A. Parks and D. N. Granger have shown that relatively little injury to the intestinal mucosa occurs during the ischemic period and that the majority of the injury occurs upon reperfusion. Evidence for the involvement of reactive oxygen metabolites in reperfusion injury is based on the use of agents that either restrict the production of oxidants or act as scavengers after the oxidants are produced. The observation that iron-loaded deferoxamine or transferrin did not protect the intestine against reperfusion injury argues against a nonspecific protective effect of these iron-binding compounds. Additional evidence in support of the theory that xanthine oxidase is an important source of reactive oxygen metabolites in postischemic intestine is provided by studies in which tissue xanthine oxidase is depleted by administration of a tungsten-supplemented, molybdenum-deficient diet.
