Lower limb ischaemia-reperfusion injury alters gastrointestinal structure and function

Yassin, M. M. I.; D’Sa, Aires A.B. Barros; Parks, T. G.; McCaigue, M. D.; Leggett, P. L.; Halliday, M. I.

doi:10.1111/j.1365-2168.1997.02772.x

Cited by 26 publications

(26 citation statements)

References 22 publications

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“…It has been demonstrated that neutrophils contribute to lung injury 26 . On the other hand, morphological changes in the intestine in response to 3 h of bilateral hind-limb ischaemia followed by 2 h of reperfusion were not associated with neutrophil in®ltration into the intestinal tissue 5 , in line with the ®ndings in the present study.…”

Section: Discussionsupporting

confidence: 79%

“…This ®nding provides a mechanism for the previously observed morphological and functional changes in the intestine in response to I-R of the leg 4,5 . In animal models of burn injury, haemorrhagic shock and endotoxaemia, diminished intestinal perfusion was associated with increased epithelial permeability 10,27,28 .…”

Section: Discussionmentioning

confidence: 99%

“…Experimental evidence suggests that the gut is an important mediator in this process. It has been demonstrated in rats that reperfusion of ischaemic hind limbs is associated with a reduction of intestinal mucosal thickness and an increase in intestinal permeability, as well as an increase in systemic endotoxin concentration 4,5 . These studies indicate that hind-limb I-R induces a loss of the intestinal barrier function, with subsequent translocation of endotoxin from the gut.…”

Section: Introductionmentioning

confidence: 99%

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Effects of experimental lower-limb ischaemia–reperfusion injury on the mesenteric microcirculation

Wehrens

Rouwet

Egbrink

et al. 2002

British Journal of Surgery

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Background: Ischaemia±reperfusion (I-R) of the leg is associated with functional and structural changes in the intestine. This study assessed whether acute hind-limb I-R in rats induced a reduction in perfusion and/or signs of an in¯ammatory response in the intestine.Methods: Rats were subjected to 2 h of unilateral hind-limb ischaemia followed by 2 h of reperfusion (I-R group, n = 9) or to a sham procedure (control group, n = 9). Mesenteric microvascular diameters, red blood cell velocity, blood¯ow and leucocyte±vessel wall interactions during reperfusion were measured using intravital microscopy.Results: Blood pressure and heart rate decreased from 30 min of reperfusion onwards in the I-R group compared with controls. From 15 min after the start of reperfusion, mesenteric arteriolar and venular red blood cell velocity and blood¯ow decreased by 40±50 per cent. Microvascular diameters and leucocyte±vessel wall interactions did not change. Conclusion:Restoration of blood¯ow to an acutely ischaemic hind limb led to a signi®cant decline in the splanchnic microcirculatory blood¯ow. There were, however, no signs of an early in¯ammatory response in the gut.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effects of experimental lower-limb ischaemia–reperfusion injury on the mesenteric microcirculation

Wehrens

Rouwet

Egbrink

et al. 2002

British Journal of Surgery

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“…Limb ischemia-reperfusion injury, leading to changes in the permeability of the intestinal mucosa, may be closely related to the production of excess oxygen free radicals (15,16,23,24). The production of reactive oxygen metabolites during ischemia-reperfusion involves oxidases found in resident phagocytic cells as well as microvascular and mucosal epithelial cells (25).…”

Section: Discussionmentioning

confidence: 99%

“…Ischemia-reperfusion injury of the gastrointestinal tract not only causes damage to the function of the gastrointestinal tract, but may also be a factor in the development of multiple organ dysfunction syndrome (MODS) associated with reperfusion injury (14,15). The results of the current study showed that at different times of reperfusion following limb ischemia, when varying degrees of small intestinal mucosal damage occurred, the small intestinal tissue DAO activity -which has been a major indicator of the integrity and functional mass of the intestinal mucosa (16) -was lower in the LIR group than in the S group (the sham-operated group).…”

Section: Discussionmentioning

confidence: 99%

Ischemic post-conditioning attenuates the intestinal injury induced by limb ischemia/reperfusion in rats

Leng¹,

Zhang²,

Zhang³

et al. 2011

Braz J Med Biol Res

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The purpose of this study was to investigate the protective effects of ischemic post-conditioning on damage to the barrier function of the small intestine caused by limb ischemia-reperfusion injury. Male Wistar rats were randomly divided into 3 groups (N = 36 each): sham operated (group S), lower limb ischemia-reperfusion (group LIR), and post-conditioning (group PC). Each group was divided into subgroups (N = 6) according to reperfusion time: immediate (0 h; T1), 1 h (T2), 3 h (T3), 6 h (T4), 12 h (T5), and 24 h (T6). In the PC group, 3 cycles of reperfusion followed by ischemia (each lasting 30 s) were applied immediately. At all reperfusion times (T1-T6), diamine oxidase (DAO), superoxide dismutase (SOD), and myeloperoxidase (MPO) activity, malondialdehyde (MDA) intestinal tissue concentrations, plasma endotoxin concentrations, and serum DAO, tumor necrosis factor-α (TNF-α), and interleukin-10 (IL-10) concentrations were measured in sacrificed rats. Chiu’s pathology scores for small intestinal mucosa were determined under a light microscope and showed that damage to the small intestinal mucosa was lower in group PC than in group LIR. In group PC, tissue DAO and SOD concentrations at T2 to T6, and IL-10 concentrations at T2 to T5 were higher than in group LIR (P < 0.05); however, tissue MPO and MDA concentrations, and serum DAO and plasma endotoxin concentrations at T2 to T6, as well as TNF-α at T2 and T4 decreased significantly (P < 0.05). These results show that ischemic post-conditioning attenuated the permeability of the small intestines after limb ischemia-reperfusion injury. The protective mechanism of ischemic post-conditioning may be related to inhibition of oxygen free radicals and inflammatory cytokines that cause organ damage

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Effect of microRNA‐26a on vascular endothelial cell injury caused by lower extremity ischemia–reperfusion injury through the AMPK pathway by targeting PFKFB3

Zhang

Xue

et al. 2018

Journal Cellular Physiology

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Vascular endothelial cell (VEC) dysfunction plays an important role in the ischemia-reperfusion injury (IRI)-related diseases, and microRNAs (miRNAs) are key factors during this process. We conducted this study to investigate whether miRNA-26a (miR-26a) has effect on the IRI-induced VEC injury via the AMPK pathway by targeting 6-phosphofructo-2-kinase-fructose-2,6-biphosphatase 3 (PFKFB3). IRI rat models were successfully constructed by an abdominal incision. Additionally, the cultured VECs were further treated with miR-26a mimic or inhibitor, and si-PFKFB3. Both the reverse-transcription quantitative polymerase chain reaction and the western blot assay method were carried out to examine the expressions of PFKFB3, endothelial nitric oxide synthase (eNOS), and 5'-adenosine monophosphate-activated protein kinase (AMPK) α1, as well as the extent of the AMPK α1 phosphorylation levels in vascular tissues. Circulating endothelial cell (CEC), von Willebrand factor (VWF), thrombomodulin (TM), superoxide dismutase (SOD), malondialdehyde (MDA), nitric oxide (NO), and endothelin (ET) were all measured. In the rat model of an IRI, a poorly expressed miR-26a and contrarily highly expressed PFKFB3 were identified in vascular tissues. In response to an overexpression of miR-26a or to the PFKFB3 gene silencing, decreased CEC number, TM, VWF, MDA, and ET contents, increased AMPK α1, and eNOS levels, as well as the extent of AMPK α1 phosphorylation coordinate with both increased SOD and NO contents based on the restoration of the AMPK pathway. Overexpression of the miR-26a or si-PFKFB3 provides an elevation in cell proliferation. Our study suggests that the miR-26a RNA alleviates lower extremity IRI-induced VEC injury in rats through the activation of the AMPK pathway by inhibiting PFKFB3.

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Lower limb ischaemia-reperfusion injury alters gastrointestinal structure and function

Abstract: These data suggest that reperfusion of acutely ischaemic extremities produces structural and functional changes in the small intestine, although these changes are not associated with increased neutrophil infiltration within the bowel wall.

Cited by 26 publications

References 22 publications

Effects of experimental lower-limb ischaemia–reperfusion injury on the mesenteric microcirculation

Effects of experimental lower-limb ischaemia–reperfusion injury on the mesenteric microcirculation

Ischemic post-conditioning attenuates the intestinal injury induced by limb ischemia/reperfusion in rats

Effect of microRNA‐26a on vascular endothelial cell injury caused by lower extremity ischemia–reperfusion injury through the AMPK pathway by targeting PFKFB3

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