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Tissue perfusion in critical illnesses. Antioxidant therapy
H J Schiller1, P M Reilly, G B Bulkley
1Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, MD.
Critical Care Medicine
|February 1, 1993
Summary
Reperfusion injury, particularly in the small intestine, is caused by free radicals generated by xanthine oxidase. Antioxidant therapies targeting free radical production show promise in preventing this injury.
Area of Science:
- Biomedical Science
- Cellular Biology
- Pathophysiology
Background:
- Reperfusion injury is a significant clinical challenge.
- Free radicals play a critical role in tissue damage following ischemia.
- The small intestine is particularly vulnerable to ischemia-reperfusion events.
Purpose of the Study:
- To elucidate the mechanisms of free radical-mediated reperfusion injury.
- To review current antioxidant strategies for preventing and treating reperfusion injury.
Main Methods:
- Literature review of studies from 1966-1991.
- Analysis of articles on free radical generation, tissue injury, and antioxidant function.
- Data abstraction from relevant publications.
Main Results:
- Ischemia activates xanthine oxidase, leading to superoxide radical burst upon reperfusion.
- Free radicals and their metabolites contribute significantly to mucosal injury.
- Endothelial cell xanthine oxidase, not epithelial, is implicated in triggering intestinal reperfusion injury.
Conclusions:
- Free radical generation is a key mechanism in reperfusion injury across multiple organs.
- Targeting free radical production at reperfusion presents a potential therapeutic avenue.
- Antioxidant therapies offer a promising strategy to mitigate reperfusion-induced tissue damage.