Alterations of intestinal motor responsiveness in a model of mild mesenteric ischemia/reperfusion in rats

Ballabeni, Vigilio; Barocelli, Elisabetta; Bertoni, Simona; Impicciatore, M

doi:10.1016/s0024-3205(02)01966-5

Cited by 58 publications

(56 citation statements)

References 30 publications

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“…The functional alterations caused by I/R have been previously identified [15] . These changes consist of reversible alterations in smooth muscle contractility and intestinal transit, as well as characteristic changes in electrical activity such as a decrease in BER frequency during ischemia [7,16] . Nitric oxide is one of the mediators thought to participate in the changes caused by I/R on intestinal motility in the rat [17] .…”

Section: Discussionmentioning

confidence: 99%

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Ketamine anesthesia reduces intestinal ischemia/reperfusion injury in rats

Cámara¹,

Guzmán²,

Barrera³

et al. 2008

WJG

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showed significantly less injury in rats that received ketamine than in rats that did not (2.35 ± 1.14 vs 4.58 ± 0.50, P < 0.0001). The distance traveled by a marker, expressed as percentage of total intestinal length, in rats that received pentobarbital sodium was 20% ± 2% in comparison with 25.9% ± 1.64% in rats that received ketamine (P = 0.017 INTRODUCTIONMesenteric ischemia is a clinical entity with a mortality rate between 60% and 100% that usually requires surgical resection of the necrotic intestinal segment [1] . Although there have been advancements in the treatment of ischemic injury, an ideal treatment has not been defined, and new options should be considered. A promising strategy is the use of anesthetic and sedative agents that might exert protective effects on the injured tissue. Ketamine is an agent that has been recommended for this purpose in clinical situations of sepsis, renal ischemia, cerebral ischemia and serious burn injuries [2][3][4] . The small intestine is very sensitive to ischemic insult [5] . Reperfusion causes additional damage through the release of free radicals, pro-inflammatory cytokines, leukotrienes and other related products [6] . Intestinal Abstract AIM: To investigate the effects of ketamine anesthesia on the motility alterations and tissue injury caused by ischemia/reperfusion in rats. METHODS: T h i r ty m a l e W i s t a r ra t s w e i g h i n g 200-250 g were used. Ischemia was induced by obstructing blood flow in 25% of the total small intestinal length (ileum) with a vascular clamp for 45 min, after which either 60 min or 24 h of reperfusion was allowed. Rats were either anesthetized with pentobarbital sodium (50 mg/kg) or ketamine (100 mg/kg). Control groups received sham surgery. After 60 min of reperfusion, the intestine was examined for morphological alterations, and after 24 h intestinal basic electrical rhythm (BER) frequency was calculated, and intestinal transit determined in all groups. RESULTS: The intestinal mucosa in rats that were anesthetized with ketamine showed moderate alterations such as epithelial lifting, while ulceration and hemorrhage was observed in rats that received pentobarbital sodium after 60 min of reperfusion. Quantitative analysis of structural damage using the Chiu scale

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Section: Discussionmentioning

confidence: 99%

“…Ketamine on ischemia/reperfusion 5193 ischemia/reperfusion (I/R) damages the intestinal mucosa and alters gastrointestinal motility [7] . The histological damage induced by I/R includes alterations in capillary permeability, mucosal barrier dysfunction, necrosis, epithelial shredding.…”

Section: Introductionmentioning

confidence: 99%

Ketamine anesthesia reduces intestinal ischemia/reperfusion injury in rats

Cámara¹,

Guzmán²,

Barrera³

et al. 2008

WJG

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“…Loss of mucosal integrity has been implicated in the pathogenesis of the multiple organ dysfunction syndrome, a life-threatening complication of intestinal ischemia, which may be caused by a hyper-inflammatory response and by the loss of autoregulation of the normal inflammatory response. 18 Alterations of gastrointestinal motility, 8,41,42 which can be partly due to structural changes and neuronal plasticity occurring within the enteric nervous system, 29,43 may also contribute to the development of bacterial overgrowth with subsequent bacterial translocation. Mast cells degranulation has been recognized as an important factor in mediating mucosal damage and motor alterations in small bowel.…”

Section: Discussionmentioning

confidence: 99%

“…1 Intestinal ischemia occurs in a wide variety of clinical manifestations, including mesenteric vascular occlusion, neonatal necrotizing enterocolitis, abdominal angina, and Crohn's disease. [2][3][4][5][6][7][8][9] Graft ischemia is also a serious complication of small bowel transplantation. 10,11 Ischemic injury due to severe loss in intestinal blood flow can result in many clinical consequences ranging from bleeding, intestinal perforation, and peritonitis to more serious systemic conditions, including myocardial and renal failure, sepsis, multiple organ dysfunction syndrome, and death.…”

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confidence: 99%

“…This experimental procedure induces transient mucosal damage and alterations of motor activity. 8,29 The aims of the study were to investigate: 1) whether PAR 2 activation with a selective PAR 2 agonist affects gastrointestinal motility impairment and mucosal damage in rats with intestinal ischemia followed by reperfusion (I/R) compared with sham-operated (SO) mice and in mice with or without deletion of the PAR 2 gene (PAR 2 Ϫ/Ϫ and PAR 2 ϩ/ϩ ); 2) the expression of PAR 2 mRNA in the intestine of I/R rats following PAR 2 activation; 3) whether the effects of PAR 2 activation on motility and tissue damage in I/R involve mast cells and extrinsic primary afferent nerves; and 4) the role of calcitonin gene-related peptide (CGRP) and substance P (SP), peptides that control inflammation and pain and colocalize with PAR 2 in visceral afferents, 27,30,31 in mediating PAR 2 effects in intestinal ischemia.…”

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confidence: 99%

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Protective Effect of Proteinase-Activated Receptor 2 Activation on Motility Impairment and Tissue Damage Induced by Intestinal Ischemia/Reperfusion in Rodents

Cattaruzza

Cenac

Barocelli

et al. 2006

The American Journal of Pathology

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We hypothesized that proteinase-activated receptor-2 (PAR 2 ) modulates intestinal injuries induced by ischemia/reperfusion. Ischemia (1 hour) plus reperfusion (6 hours) significantly delayed gastrointestinal transit (GIT) compared with sham operation. Intraduodenal injection of PAR 2 -activating peptide SLIGRL-NH 2 significantly accelerated transit in ischemia/reperfusion but not in sham-operated rats. GIT was significantly delayed in ischemia/reperfusion and sham-operated PAR 2 ؊/؊ mice compared with PAR 2 ؉/؉ . SLIGRL-NH 2 significantly accelerated transit in ischemia/reperfusion in PAR 2 ؉/؉ but not in PAR 2 ؊/؊ mice. Prevention of mast cell degranulation with cromolyn, ablation of visceral afferents with capsaicin, and antagonism of calcitonin generelated peptide (CGRP) and neurokinin-1 receptors with CGRP 8 -37 and RP67580, respectively, abolished the SLIGRL-NH 2 -induced stimulatory effect on transit in ischemia/reperfusion. Tissue damage was significantly reduced by SLIGRL-NH 2 ; this effect was not observed in cromolyn-, capsaicin-, or RP67580-treated rats but was detected following CGRP 8 -37 . Intestinal PAR 2 mRNA levels were not affected by SLIGRL-NH 2 in ischemia/reperfusion. We propose that PAR 2 modulates GIT and tissue damage in intestinal ischemia/reperfusion by a mechanism dependent on mast cells and visceral afferents. PAR 2 effect on transit might be mediated by CGRP and substance P, whereas the effect on tissue damage appears to involve substance P but not CGRP. PAR 2 might be a signaling system in the neuroimmune communication in intestinal ischemia/reperfusion.

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Protective role of μ opioid receptor activation in intestinal inflammation induced by mesenteric ischemia/reperfusion in mice

Saccani

Anselmi

Jaramillo

et al. 2012

J of Neuroscience Research

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Intestinal ischemia is a clinical emergency with high morbidity and mortality. We investigated whether activation of µ opioid receptor (µOR) protects from the inflammation induced by intestinal ischemia and reperfusion (I/R) in mice. Ischemia was induced by occlusion of the superior mesenteric artery (45 min) and followed by reperfusion (5 hours). Sham Operated (SO) and normal (N) mice served as controls. Each group received subcutaneously: (1) saline solution; (2) the µOR selective agonist, [D-Ala2, N-Me-Phe4, Gly5-ol]-enkephalin (DAMGO) (0.01 mg.kg−1); (3) DAMGO and the selective µOR antagonist [H-D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2] (CTAP) (0.1 mg.kg−1) or (4) CTAP alone. I/R induced intestinal inflammation as indicated by histological damage and the significant increase in myeloperoxidase (MPO) activity, index of tissue neutrophil accumulation. TNF-α and IL-10 mRNA levels were also increased in I/R mice compared to SO. DAMGO significantly reduced tissue damage, MPO activity and TNF-α mRNA levels in I/R and these effects were reversed by CTAP. By contrast, DAMGO did not modify IL-10 mRNA levels and gastrointestinal transit. DAMGO effects are receptor-mediated and are likely due to activation of peripheral µORs since it does not readily cross the blood brain barrier. These findings suggest that activation of peripheral µOR protects from the inflammatory response induced by I/R through a pathway involving the pro-inflammatory cytokine, TNF-α. Reduction of acute inflammation might prevent I/R complications, including motility impairment, which develop at a later stage of reperfusion and are likely due to inflammatory cell infiltrates.

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Alterations of intestinal motor responsiveness in a model of mild mesenteric ischemia/reperfusion in rats

Cited by 58 publications

References 30 publications

Ketamine anesthesia reduces intestinal ischemia/reperfusion injury in rats

Ketamine anesthesia reduces intestinal ischemia/reperfusion injury in rats

Protective Effect of Proteinase-Activated Receptor 2 Activation on Motility Impairment and Tissue Damage Induced by Intestinal Ischemia/Reperfusion in Rodents

Protective role of μ opioid receptor activation in intestinal inflammation induced by mesenteric ischemia/reperfusion in mice

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