| pubmed-article:18437208 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18437208 | lifeskim:mentions | umls-concept:C0003402 | lld:lifeskim |
| pubmed-article:18437208 | lifeskim:mentions | umls-concept:C0017189 | lld:lifeskim |
| pubmed-article:18437208 | lifeskim:mentions | umls-concept:C0242606 | lld:lifeskim |
| pubmed-article:18437208 | lifeskim:mentions | umls-concept:C0035126 | lld:lifeskim |
| pubmed-article:18437208 | lifeskim:mentions | umls-concept:C0033613 | lld:lifeskim |
| pubmed-article:18437208 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:18437208 | pubmed:dateCreated | 2008-4-25 | lld:pubmed |
| pubmed-article:18437208 | pubmed:abstractText | Exacerbation of hypoxic injury after reoxygenation is a crucial mechanism mediating organ injury in transplantation, and in myocardial, hepatic, gastrointestinal, cerebral, renal, and other ischemic syndromes. The occlusion and reperfusion of the splanchnic artery is a useful animal model to elucidate the mechanism of gastrointestinal injury induced by ischemia-reperfusion (I/R). Although xanthine oxidase is a major source of reactive oxygen species (ROS), which plays an important role in the I/R-induced intestinal injury, there are many other sources of intracellular ROS. Various treatment modalities have been successfully applied to attenuate the I/R injury in animal models. This review focuses on the role of oxidant stress in the mechanism of I/R injury and the use of antioxidant agents for its treatment. | lld:pubmed |
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