Reperfusion injury after intestinal ischemia

Schoenberg, M. H.; Beger, H. G.

doi:10.1097/00003246-199309000-00023

Cited by 264 publications

(72 citation statements)

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“…These are the enhanced generation of oxygen radicals and the activation of phospholipase A 2 . 27 Lipid based cell membranes are the primary target of oxygen derived free radicals. They react directly with polyunsaturated fatty acids, leading to lipid peroxidation within the cell membranes followed by disintegration of the cells and ultimately to cell death.…”

Section: Discussionmentioning

confidence: 99%

“…27 SOD is a protective enzyme that e ciently and speci®cally scavenges the superoxide radicals by catalyzing their dismutation to hydrogen peroxide and oxygen. On the other hand, catalase is an enzyme that enhances the degradation of hydrogen peroxide to oxygen and water.…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, catalase is an enzyme that enhances the degradation of hydrogen peroxide to oxygen and water. 27 Hence, determining the concentrations of these enzymes in tissue will indirectly give some idea about free radical formation following an ischemic insult. Our data also support this idea, and the levels of SOD and CAT in all groups correlated well with MDA levels.…”

Section: Discussionmentioning

confidence: 99%

“…It is documented that free radicals are generated within the ®rst minutes of reperfusion when oxygen reaches the ischemic organ. 27 In a rabbit model of spinal cord IR injury, it has been shown that lipid peroxidation reaches its peak level by 4 h of reperfusion. 2 Leukocyte accumulation has also been shown to occur in a few hours after the onset of ischemia and to be coincident with the development of postischemic hypoperfusion and progressive neuronal death.…”

Section: Discussionmentioning

confidence: 99%

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Pentoxifylline reduces biochemical markers of ischemia-reperfusion induced spinal cord injury in rabbits

et al. 2002

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Study design: Occlusion of the infrarenal abdominal aorta with administration of pentoxifylline was applied to adult rabbits, followed by removal of aortic clamp and reperfusion. Tissue levels of cytokines, lipid peroxides, and antioxidant enzymes were assayed and compared within groups. Objectives: To examine the e ect of pentoxifylline (PTX) on cytokine levels, lipid peroxidation, and antioxidant enzymes in a rabbit model of spinal cord ischemia-reperfusion injury induced by aortic occlusion. Setting: Isparta, Turkey. Methods: Rabbits were randomly allocated into four groups of sham laparotomy (SHAM), sham laparotomy with PTX administration (SHAM+PTX), aortic occlusion and reperfusion (AOR), aortic occlusion and reperfusion with PTX administration (AOR+PTX). An intravenous bolus of 50 mg/kg PTX was given just before aortic cross clamping. An atraumatic microvascular clamp was then placed on the abdominal aorta immediately distal to the left renal artery for 30 min. PTX was infused at a rate of 0.5 mg/kg/min during the aortic occlusion. Animals were subjected to 120 min of reperfusion after removal of the aortic clamp. All animals were sacri®ced at the end of reperfusion. The lumbosacral segments of spinal cords were quickly harvested and stored at 7788C for biochemical assays of IL-6, TNF-a, MDA, SOD, and CAT levels. Di erences among groups were analyzed by one-way analysis of variance followed by a post hoc Tukey's honestly signi®cant di erence test. Results: No di erences in mean levels of IL-6, TNF-a, MDA, SOD, and CAT were noted between SHAM and SHAM+PTX groups (P40.05). There was a signi®cant increase in all biochemical parameters in the AOR group (P50.05). Administration of PTX signi®cantly attenuated the levels of all biochemical parameters in the AOR+PTX group (P50.05). Conclusion: PTX pretreatment attenuated ischemia-reperfusion induced spinal cord injury in a rabbit model, in terms of biochemical parameters of ischemia and reperfusion.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Pentoxifylline reduces biochemical markers of ischemia-reperfusion induced spinal cord injury in rabbits

et al. 2002

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“…Intestinal I/R manifests as damage to the intestinal mucosa, which is characterised by increased vascular permeability and intestinal oedema, increased mucosal permeability and barrier dysfunction, combined with haemodynamic and cardiovascular changes (Schoenberg & Beger, 1993;Khanna et al, 2001). The local effect in the intestine is coupled with injury to remote organs and in some cases the onset of sepsis and multiple organ failure (Poggetti et al, 1992;Harward et al, 1993;Moore et al, 1994;Turnage et al, 1996;Carden & Granger, 2000).…”

Section: Introductionmentioning

confidence: 99%

Comparative anti‐inflammatory activities of antagonists to C3a and C5a receptors in a rat model of intestinal ischaemia/reperfusion injury

Proctor

Shiels

Reid

et al. 2004

British J Pharmacology

101

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1 Complement activation is implicated in the pathogenesis of intestinal ischaemia-reperfusion injury (I/R), although the relative importance of individual complement components is unclear. A C3a receptor antagonist N(2)-[(2,2-diphenylethoxy)acetyl]-L-arginine (C3aRA) has been compared with a C5a receptor antagonist (C5aRA), AcF-[OPdChaWR], in a rat model of intestinal I/R. 2 C3aRA (IC 50 ¼ 0.15 mM) and C5aRA (IC 50 ¼ 0.32 mM) bound selectively to human polymorphonuclear leukocyte (PMN) C3a and C5a receptors, respectively. Effects on circulating neutrophils and blood pressure in the rat were also assessed. 3 Anaesthetised rats, subjected to intestinal ischaemia (30 min) and reperfusion (120 min), were administered intravenously with either (A) the C3aRA (0.1-1.0 mg kg À1 ); the C5aRA (1.0 mg kg À1 ); the C3aRA þ C5aRA (each 1.0 mg kg À1 ); or vehicle, 45 min prior, or (B) the C3aRA (1.0 mg kg À1 ) or vehicle, 120 min prior to reperfusion. 4 The C3aRA and C5aRA, administered 45 min prior to reperfusion, displayed similar efficacies at ameliorating several disease markers (increased oedema, elevated ALT levels and mucosal damage) of rat intestinal I/R. The combination drug treatment did not result in greater injury reduction than either antagonist alone. However, doses of the C3aRA (0.01-10 mg kg À1 ) caused transient neutropaenia, and the highest dose (10 mg kg À1 ) also caused a rapid and transient hypertension. 5 The C3aRA (1.0 mg kg À1 ), delivered 120 min prior to reperfusion to remove the global effect of C3aRA-induced neutrophil sequestration, did not attenuate the markers of intestinal I/R, despite persistent C3aR antagonism at this time. 6 C3aR antagonism does not appear to be responsible for the anti-inflammatory actions of this C3aRA in intestinal I/R in the rat. Instead, C3aRA-mediated global neutrophil tissue sequestration during ischaemia and early reperfusion may account for the protective effects observed.

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Acute Mesenteric Ischemia

et al. 2004

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Acute mesenteric ischemia is a life-threatening vascular emergency that requires early diagnosis and intervention to adequately restore mesenteric blood flow and to prevent bowel necrosis and patient death. The underlying cause is varied, and the prognosis depends on the precise pathologic findings. Despite the progress in understanding the pathogenesis of mesenteric ischemia and the development of modern treatment modalities, acute mesenteric ischemia remains a diagnostic challenge for clinicians, and the delay in diagnosis contributes to the continued high mortality rate. Early diagnosis and prompt effective treatment are essential to improve the clinical outcome.

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Reperfusion injury after intestinal ischemia

Cited by 264 publications

References 0 publications

Pentoxifylline reduces biochemical markers of ischemia-reperfusion induced spinal cord injury in rabbits

Pentoxifylline reduces biochemical markers of ischemia-reperfusion induced spinal cord injury in rabbits

Comparative anti‐inflammatory activities of antagonists to C3a and C5a receptors in a rat model of intestinal ischaemia/reperfusion injury

Acute Mesenteric Ischemia

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