Abstract
Background: We have shown that both intra-ischemic hypothermia and hypertonic saline resuscitation provide dramatic protection against gut ischemia/reperfusion (I/R) injury that is in part mediated by HO-1. We, therefore, hypothesized that induction of HO-1 by hemin would lessen mucosal damage and improve function after gut I/R. Methods: Rats underwent superior mesenteric artery occlusion (SMAO) for 60 min or sham laparotomy. Animals were pretreated with hemin (HO-1 inducer Ferric Protoporphyrin IX chloride) 50 μmol/kg sq two hours prior to SMAO or sham laparotomy. Six hours after reperfusion, transit was determined by quantitation of % tracer in 10 segments of small intestine 30 min following injection into the duodenum (expressed as mean geometric center). Ileum was harvested for mucosal histological injury (Chiu score 0–5 by blinded observer) and for HO-1 protein expression. Data expressed as mean ± SEM, ANOVA (n = 6/group). Means with different superscripts are significantly different. Results: Hemin significantly induced HO-1 expression in sham/hemin (0.34 ± 0.09) compared to sham alone (0 ± 0) and in SMAO/hemin (0.69 ± 0.2) compared to SMAO alone (0.46 ± 0.05). Hemin did not effect transit in sham/hemin, but significantly improved impaired transit after SMAO/hemin (Fig). Hemin did not cause mucosal injury in sham/hemin (0.3 ± 0.2) compared to sham alone (0 ± 0) but did significantly decrease damage after SMAO/hemin (2.3 ± 0.5) compared to SMAO alone (4.6 ± 0.4). Conclusion: These data support our hypothesis HO-1 plays an important role in protecting the gut against I/R injury.
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