Ischemia and reperfusion of the ischemic intestine can result in significant tissue injury that is manifested as vascular dysfunction and mucosal barrier failure. The injury response to ischemia per se can be attributed to hypoxia and the cellular alterations brought about by this condition. Several protective mechanisms, including intramural and extramural collaterals, arteriolar dilation, and capillary recruitment, exist to minimize the reduction in tissue oxygen tension that accompanies partial occlusion of the arterial supply to the intestine. Reperfusion of the ischemic intestine is accompanied by a more profound injury response that has been linked to the generation of reactive oxygen species that are derived from the enzyme xanthine oxidase. The accumulation of these reactive species at the time of reperfusion, coupled with the inactivation of nitric oxide, creates an inflammatory phenotype within the vasculature and mucosal membrane. The resulting recruitment of leukocytes and platelets and the activation of resident inflammatory cells that normally reside in the perivascular space (mast cells, macrophages) lead to further oxidative stress and a more intense inflammatory condition, ultimately resulting in capillary and mucosal membrane failure and organ dysfunction.
|Original language||English (US)|
|Title of host publication||PanVascular Medicine, Second Edition|
|Publisher||Springer Berlin Heidelberg|
|Number of pages||19|
|State||Published - Jan 1 2015|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)