The Influence of Ischemia/Reperfusion Injury on the Jejunum

Blennerhassett, Lewis; Kong, Sung‐Eun; Heel, Kathy; Mccauley, Rosalie; Hall, John C.

doi:10.1097/00000637-199806000-00008

Cited by 7 publications

(5 citation statements)

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“…This is consistent with our previous characterization of this animal model. 20 It should also be noted that this finding is in accord with the underlying processes that culminate in cellular necrosis. The induction of apoptosis associated with intestinal IRI begins within an hour of reperfusion and is probably responsible for the observed crypt and villous loss.…”

Section: Discussionsupporting

confidence: 62%

“…24 Glutaminase activity is a measure of the preservation of functional enterocytes after IRI. Blennerhasset et al 20 showed that the mucosal activity of glutaminase was reduced after an ischemic insult and was reduced even further after a period of reperfusion. It is of interest that Basoglu et al 25 reported that parenteral glutamine supplementation protects the small intestine of albino rabbits from IRI, possibly because glutamine plays a regulatory role in the biosynthesis of glutathione and nitric oxide.…”

Section: Discussionmentioning

confidence: 99%

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Influence of glycine on intestinal ischemia‐reperfusion injury

Lee

Mccauley²,

Kong

et al. 2002

J Parenter Enteral Nutr

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Section: Discussionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Influence of glycine on intestinal ischemia‐reperfusion injury

Lee

Mccauley²,

Kong

et al. 2002

J Parenter Enteral Nutr

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“…IL-6 is known to be induced in the gut early in the postischemic phase and to participate in the inflammatory response (15). ICAM-1 is an adhesion molecule that is induced by various inflammatory mediators and plays an important role in gut ischemia-reperfusioninduced mucosal dysfunction and neutrophil infiltration (5,34). Both of these proteins are regulated in part by NF-B.…”

Section: Bay 11-7085 Protects Against Early But Exacerbates Late Mementioning

confidence: 99%

Effects of NF-κB inhibition on mesenteric ischemia-reperfusion injury

Zou

Attuwaybi²,

Kone

2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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Mesenteric ischemia-reperfusion injury is a serious complication of shock. Because activation of nuclear factor-kappaB (NF-kappaB) has been implicated in this process, we treated rats with vehicle or the IkappaB-alpha inhibitor BAY 11-7085 (25 mg/kg ip) 1 h before mesenteric ischemia-reperfusion (45 min of ischemia followed by reperfusion at 30 min or 6 h) and examined the ileal injury response. Vehicle-treated rats subjected to ischemia-reperfusion exhibited severe mucosal injury, increased myeloperoxidase (MPO) activity, increased expression of interleukin-6 and intercellular adhesion molecule 1 protein, and a biphasic peak of NF-kappaB DNA-binding activity during the 30-min and 6-h reperfusion courses. In contrast, BAY 11-7085-pretreated rats subjected to ischemia-reperfusion exhibited less histological injury and less interleukin-6 and intercellular adhesion molecule 1 protein expression at 30 min of reperfusion but more histological injury at 6 h of reperfusion than vehicle-treated rats subjected to ischemia-reperfusion. Studies with phosphorylation site-specific antibodies demonstrated that IkappaB-alpha phosphorylation at Ser(32),Ser(36) was induced at 30 min of reperfusion, whereas tyrosine phosphorylation of IkappaB-alpha was induced at 6 h of reperfusion. BAY 11-7085 inhibited the former, but not the latter, phosphorylation pathway, whereas alpha-melanocyte-stimulating hormone, which is effective in limiting late ischemia-reperfusion injury to the intestine, inhibited tyrosine phosphorylation of IkappaB-alpha. Thus NF-kappaB appears to play an important role in the generation and resolution of intestinal ischemia-reperfusion injury through different activation pathways.

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“…This phenomenon is well-documented, and is referred to as ischemia-reperfusion injury (IRI) [3][4][5][6]. IRI is a distinct entity from ischemia alone, and it is thought to be due to a complex interplay of oxidative and inflammatory processes that result in the release of toxic metabolites and subsequent endothelial injury and microvascular thrombosis [7].…”

Section: Introductionmentioning

confidence: 99%