Journal
JOURNAL OF SURGICAL RESEARCH
Volume 118, Issue 1, Pages 53-57Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.jss.2004.01.010
Keywords
hemin; heme oxygenase-1; ischemia/reperfusion; superior mesenteric artery occlusion; intestinal transit
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Funding
- NIGMS NIH HHS [T32 GM 08792, P50 GM38529] Funding Source: Medline
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Background. We have shown that both intraischemic hypothermia and hypertonic saline resuscitation provide dramatic protection against gut ischemia/reperfusion (I/R) injury that is in part mediated by heme oxygenase-1 (HO-1). We therefore hypothesized that induction of HO-1 by hemin would lessen damage and improve function after gut I/R. Materials and methods. Male Sprague-Dawley rats were treated with 50 mumol/kg hemin (HO-1 inducer ferric protoporphyrin IX chloride) sq or vehicle 2 h before superior mesenteric artery occlusion for 60 min or sham laparotomy. After 6 h of reperfusion, transit was determined by quantitation of percentage of tracer in 10 equal segments of small intestine 30 min following injection into the duodenum (expressed as mean geometric center). Ileum was harvested for assessment of mucosal histologic injury (Chin score 0-5 by blinded observer), myeloperoxidase activity (MPO, index of inflammation), and HO-1 protein expression. Results. Hemin treatment was associated with increased HO-1 protein expression, lessened mucosal injury, decreased MPO activity, and improved intestinal transit following gut I/R. Conclusion. These data corroborate that HO-1 plays an important role in protecting the gut against I/R-induced injury. (C) 2004 Elsevier Inc. All rights reserved.
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