Allopurinol and superoxide dismutase protect against leucocyte–endothelium interactions in a novel model of colonic ischaemia–reperfusion

Riaz, Amjid; Wan, Ming; Schäfer, T.; Dawson, Peter; Menger, Michael D.; Jeppsson, Bengt; Thorlacius, Henrik

doi:10.1046/j.1365-2168.2002.02279.x

Cited by 47 publications

(39 citation statements)

References 32 publications

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“…5,31 In our study, intestinal I/R injury was associated with a significant decrease of SOD activity, a major endogenous antioxidant enzyme, and increase of the lipid peroxidation product MDA in the injury group. Treatment with propofol increased SOD activity and attenuated MDA production that was associated with a reduced Chiu's score (Table).…”

Section: Discussionmentioning

confidence: 93%

“…5 The intestinal I/R injury was associated with dramatic increases in the intestinal mucosa, of MDA, ET-1, NO and LD, and a decrease in SOD activity. The novel finding of the current study is that propofol, at a sedative dosage, significantly attenuated SMA occlusion -reperfusion induced intestinal mucosal damage and the above mentioned biochemical changes when given either prior to, during SMA occlusion, or during the early phase of reperfusion.…”

Section: Discussionmentioning

confidence: 99%

“…Reactive oxygen species (ROS)-induced lipid peroxidation is known to be one of the major factors causing intestinal I/R injury, and the administration of free radical scavengers appears to prevent intestinal mucosa from intestinal I/R injury. 5 We have recently shown that antioxidant intervention during cardiac surgery under CPB attenuated gastric and intestinal mucosa injury and resulted in ameliorated postoperative myocardial injury, 6 suggesting that antioxidant intervention can attenuate intestinal I/R injury in the clinical setting. Propofol is an iv anesthetic with antioxidant properties 7,8 that is commonly used during cardiac surgery and postoperative sedation.…”

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confidence: 99%

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Propofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the rat

Liu

Rinne

et al. 2007

Can J Anesth/J Can Anesth

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Purpose:We investigated whether propofol at a sedative dose can prevent intestinal mucosa ischemia/reperfusion (I/R) injury, and if propofol can attenuate oxidative stress and increases in nitric oxide (NO) and endothelin-1 (ET-1) release that may occur during intestinal I/R injury. Methods:Rats were randomly allocated into one of five groups (n = 10 each): (i) sham control; (ii) injury (one hour superior mesenteric artery occlusion followed by three hours reperfusion); (iii) propofol pre-treatment, with propofol given 30 min before inducing intestinal ischemia; (iv) simultaneous propofol treatment, with propofol given 30 min before intestinal reperfusion was started; (v) propofol post-treatment, with propofol given 30 min after intestinal reperfusion was initiated. In the treatment groups, propofol 50 mg·kg -1 was administrated intraperitoneally. Animals in the control and untreated injury groups received equal volumes of intralipid (the vehicle solution of propofol) intraperitoneally. Intestinal mucosa histology was analyzed by Chiu's scoring assessment. Levels of lactic acid (LD), NO, ET-1, lipid peroxidation product malondialdehyde (MDA) and superoxide dismutase (SOD) activity in intestinal mucosa were determined. Results:Histological results showed severe damage in the intestinal mucosa of the injury group accompanied by increases in MDA, NO and ET-1 and a decrease in SOD activity. Propofol treatments, especially pre-treatment, significantly reduced Chiu's scores and levels of MDA, NO, ET-1 and LD, while restoring SOD activity. Conclusion:These findings indicate that propofol attenuates intestinal I/R-induced mucosal injury in an animal model. The response may be attributable to propofol's antioxidant properties, and the effects of inhibiting over-production of NO and in decreasing ET-1 levels. CAN J ANESTH 2007 / 54: 5 / pp 366-374 Objectif : Nous avons cherché à savoir si le propofol, en dose sédative, pouvait empêcher les lésions d'ischémie/reperfusion (I/R) de la muqueuse intestinale, et s'il pouvait atténuer le stress oxydatif et les augmentations dans la libération d'oxyde nitrique (NO) et d'endothéline-1 (ET-1) pouvant survenir lors de lésions I/R intestinales. Méthode : Des rats ont été randomisés en cinq groupes (n = 10 chacun) : (i) faux témoin (sham control) ; (ii) lésion (occlusion de

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Propofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the rat

Liu

Rinne

et al. 2007

Can J Anesth/J Can Anesth

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“…Xanthine Oxidase and Splanchnic Ischemia-Reperfusion. Allopurinol pretreatment is protective in the ischemic and reperfused gut and beneficially affects the changes in vascular permeability (Parks et al, 1982;Parks and Granger, 1983;Granger et al, 1986;Kulah et al, 2004), neutrophil infiltration (Grisham et al, 1986;Riaz et al, 2002), bacterial translocation (Deitsch et al, 1988;Vaughan et al, 1992), intestinal inflammatory chemokine levels (Riaz et al, 2003), motility (Hakguder et al, 2002), and mortality (Megison et al, 1990). Most of the early studies are reviewed in Schoenberg and Beger (1993).…”

Section: Therapeutic Effects Of Xanthine Oxidase Inhibitorsmentioning

confidence: 99%

Therapeutic Effects of Xanthine Oxidase Inhibitors: Renaissance Half a Century after the Discovery of Allopurinol

2006

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“…Reperfusion of ischemic tissues paradoxically exacerbates the injury process and leads to the release of reactive oxygen species and proinflammatory mediators and the attraction of inflammatory cells infiltrating the tissues (Chamoun et al, 2000;Piper et al, 2003). In the gastrointestinal tract, I/R injuries are known to be associated with significant morbidity and mortality during the course of hemorrhagic shock, abdominal aortic aneurysm repair, ischemic bowel disease, and necrotizing enterocolitis (Yasue et al, 1992;Riaz et al, 2002;Dimmitt et al, 2003).…”

mentioning

confidence: 99%

Roles of Cyclooxygenase-2 and Prostacyclin/IP Receptors in Mucosal Defense against Ischemia/Reperfusion Injury in Mouse Stomach

Kotani

Kobata²,

Nakamura³

et al. 2005

J Pharmacol Exp Ther

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We examined the roles of cyclooxygenase (COX) isozymes, prostaglandins (PGs), and their receptors in the mucosal defense against ischemia/reperfusion (I/R)-induced gastric lesions in mice. Male C57BL/6 mice, including wild-type animals and those lacking prostaglandin E 2 (EP)1, EP3, or prostaglandin I 2 (IP) receptors, were used after 18 h of fasting. Under urethane anesthesia, the celiac artery was clamped (ischemia) for 30 min, and then reperfusion was achieved for 60 min through the removal of the clamp, and the stomach was examined for lesions. I/R produced hemorrhagic gastric lesions in wild-type mice. The severity of lesions was significantly increased by pretreatment with indomethacin (a nonselective COX inhibitor) and rofecoxib (a selective COX-2 inhibitor) but not 5-(4-chlorophenyl)-1-(4-methoxyphenyl)-3-(trifluoromethyl)-1H-pyrazole (SC-560; a selective COX-1 inhibitor). The expression of COX-2 mRNA was up-regulated in the stomach following I/R but not by sham operation or ischemia alone. The ulcerogenic response was markedly aggravated in IP receptor knockout mice but not those lacking EP1 or EP3 receptors. I/R increased the levels of 6-keto-PGF 1␣ and PGE 2 in the stomach of wildtype mice, and this response was attenuated by indomethacin and rofecoxib but not SC-560. Pretreatment of wild-type mice with iloprost, a prostacyclin (PGI 2 ) analog, significantly prevented the I/R-induced gastric lesions in the absence and presence of indomethacin or rofecoxib. PGE 2 also reduced the severity of I/R-induced gastric lesions, yet the effect was much less pronounced than that of iloprost. These results suggest that endogenous PGs derived from COX-2 play a crucial role in gastric mucosal defense during I/R, and this action is mainly mediated by PGI 2 through the activation of IP receptors.

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Allopurinol and superoxide dismutase protect against leucocyte–endothelium interactions in a novel model of colonic ischaemia–reperfusion

Abstract: A new method for examining I/R-induced leucocyte responses in the colonic microcirculation is described. Oxygen free radicals play an important role in triggering leucocyte rolling and adhesion in colonic venules.

Cited by 47 publications

References 32 publications

Propofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the rat

Propofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the rat

Therapeutic Effects of Xanthine Oxidase Inhibitors: Renaissance Half a Century after the Discovery of Allopurinol

Roles of Cyclooxygenase-2 and Prostacyclin/IP Receptors in Mucosal Defense against Ischemia/Reperfusion Injury in Mouse Stomach

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