Protective Effect of Acetaminophen against Acute Gastric Mucosal Lesions Induced by Ischemia-Reperf usion in the Rat

Nakamoto, Kentaro; Kamisaki, Yoshínori; Wada, Kouichirou; Kawasaki, Hironaka; Itoh, Tadao

doi:10.1159/000139488

Cited by 21 publications

(16 citation statements)

References 23 publications

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“…4 It is known that the generation of O 2 À and H 2 O 2 during reperfusion of ischemic stomach is mediated by the xanthine/xanthine oxidase system. It has been suggested that the generation of ROM during ischemiareperfusion in stomachs is mediated not only by the xanthine/xanthine oxidase system but also by polymorphonuclear leukocytes (PMN).…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3] Reactive oxygen metabolites (ROM) have been reported to play an important role in the pathogenesis of gastric erosions induced by ischemia-reperfusion in rats. [4][5][6] Primary sources of ROM seem to be the xanthine/xanthine oxidase system and neutrophils accumulating within the reperfused tissue. ROM cause endothelial dysfunction during the early stages of reperfusion, leading to a cascade of events, including leukocyte adhesion and increased vascular permeability which contribute to organ damage.…”

Section: Introductionmentioning

confidence: 99%

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Effects ofL-carnitine on neutrophil-mediated ischemia–reperfusion injury in rat stomach

Derın

Ağaç

Bayram

et al. 2006

Cell Biochem. Funct.

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Reactive oxygen metabolites play an important role in ischemia-reperfusion related gastric injury. Primary sources of reactive oxygen metabolites seem to be the xanthine/xanthine oxidase system and neutrophils accumulating within the reperfused tissue. Tissue myeloperoxidase activity is an important index of neutrophil accumulation. The purpose of the present study was to clarify the effect of L-carnitine on the accumulation of neutrophils and neutrophil-induced gastric mucosal damage in rats exposed to ischemia-reperfusion. Rats were randomly divided into three groups: sham-operated, ischemia-reperfusion and ischemia-reperfusion plus L-carnitine groups. Ischemia was induced by clamping the celiac artery for 30 min and then reperfusion was established for 60 min. Gastric injury was assessed by measuring myeloperoxidase activity in gastric tissue. The neutrophil accumulation and hemorrhagic lesions due to ischemia-reperfusion in gastric mucosa were ascertained in a histological study. L-Carnitine (100 mg kg(-1)) administrated intravenously 5 min before ischemia significantly reduced both the gastric injury and myeloperoxidase activity compared with the ischemia-reperfusion group. The results suggest that L-carnitine provides marked protection against ischemia-reperfusion-related gastric injury which could be due to its ability to reduce neutrophil accumulation in ischemic tissue.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects ofL-carnitine on neutrophil-mediated ischemia–reperfusion injury in rat stomach

Derın

Ağaç

Bayram

et al. 2006

Cell Biochem. Funct.

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“…The recent literature, however, suggests that investigators are beginning to fill this void. For example, Nakamoto et al (22) reported beneficial effects of acetaminophen against gastric mucosal injury caused by ischemia-reperfusion in the rat. Farquhar et al (10) reported reduced renal dysfunction in the stressed human kidney in the presence of acetaminophen vs. ibuprofen, and Colletti et al (7) found that ibuprofen caused significantly greater renal arterial vasoconstriction than acetaminophen in sodium-depleted dogs.…”

mentioning

confidence: 99%

Acetaminophen and low-flow myocardial ischemia: efficacy and antioxidant mechanisms

Merrill

2002

American Journal of Physiology-Heart and Circulatory Physiology

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Merrill, Gary F. Acetaminophen and low-flow myocardial ischemia: efficacy and antioxidant mechanisms. Am J Physiol Heart Circ Physiol 282: H1341-H1349, 2002; 10.1152/ajpheart.00716.2001.-In the current study, the cardioprotective efficacy of 0.35 mmol/l acetaminophen administered 10 min after the onset of a 20-min period of global, low-flow myocardial ischemia was investigated. Matched control hearts were administered an equal volume of KrebsHenseleit physiological buffer solution (vehicle). In separate groups of hearts, the concentration-dependent, negative inotropic properties of hydrogen peroxide and the ability of acetaminophen to attenuate these actions, as well as the effects of acetaminophen on ischemia-reperfusion-mediated protein oxidation, were studied. Acetaminophen-treated hearts regained a significantly greater fraction of baseline, preischemia control function during reperfusion than vehicle-treated hearts. For example, contractility [rate of maximal developed pressure in the left ventricle (ϮdP/dtmax)] after 10 min of reperfusion was 109 Ϯ 24 and 42 Ϯ 9 mmHg/s (P Ͻ 0.05), respectively, in the two groups. The corresponding pressure-rate products were 1,840 Ϯ 434 vs. 588 Ϯ 169 mmHg ⅐ beats ⅐ min Ϫ1 (P Ͻ 0.05). Acetaminophen attenuated peroxynitrite-mediated chemiluminescence in the early minutes of reperfusion (e.g., at 6 min, corresponding values for peak light production were ϳ8 ϫ 10 6 counts/min for vehicle vs. Ͻ4 ϫ 10 6 counts/min for acetaminophen, P Ͻ 0.05) and the negative inotropic effects of exogenously administered hydrogen peroxide (e.g., at 0.4 mmol/l hydrogen peroxide, pressure-rate products were ϳ1.0 ϫ 10 4 and 3.8 ϫ 10 3 mmHg ⅐ beats ⅐ min Ϫ1 in acetaminophen-and vehicle-treated hearts, respectively, P Ͻ 0.05). Ischemia-mediated protein oxidation was reduced by acetaminophen. The ability of acetaminophen to attenuate the damaging effects of peroxynitrite and hydrogen peroxide and to limit protein oxidation suggest antioxidant mechanisms are responsible for its cardioprotective properties during postischemia-reperfusion. coronary circulation; ventricular function; peroxynitrite; hydrogen peroxide ACETAMINOPHEN WAS INTRODUCED into Western medicine more than 100 years ago, and its pain-relieving and temperature-lowering actions have been under investigation for several decades (1, 9, 26). Potential cardiovascular properties of acetaminophen have gone undiscovered, in part, because no one has made an effort to do the experiments. This might have been influenced by standard textbooks of pharmacology that report that acetaminophen lacks efficacy in the cardiovascular system of mammals (12). The recent literature, however, suggests that investigators are beginning to fill this void. For example, Nakamoto et al. (22) reported beneficial effects of acetaminophen against gastric mucosal injury caused by ischemia-reperfusion in the rat. Farquhar et al. (10) reported reduced renal dysfunction in the stressed human kidney in the presence of acetaminophen vs. ibuprofen, and Colletti et al. (7) fou...

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“…Free oxygen radicals are recognized as important mediators of gastric mucosal injury induced by gastric I/R (Kitano et al, 1997;Nakamoto et al, 1997). Lipid peroxidation is one of the major outcomes of free radical-mediated which directly damages membranes and initiates a number of secondary products including aldehydes, such as MDA, 4-hydroxy-2-nonenal, ketones, etc.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of rutin against acute gastric mucosal lesions induced by ischemia-reperfusion

Liu

Gou

et al. 2013

Pharmaceutical Biology

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Context: Rutin, a flavonoid commonly present in onions, apples and tea, has been suggested to have a variety of pharmacological activities, including immunomodulator, anti-inflammatory and antioxidant activities. Objectives: The present study was to examine the protective effects of rutin on gastric mucosal damage induced by gastric ischemia-reperfusion (I/R) in rats. Materials and methods: Rutin (50, 100, 200 mg/kg) was administered intragastrically for five consecutive days before ischemia. Sixty minutes after the last administration of rutin, under anesthesia, the celiac artery was clamped for 30 min, and then the clamp was removed for 60 min reperfusion. After reperfusion, the stomach was removed for biochemical and histological examinations. Results: As compared with the I/R group (116.7 AE 21.5), administration of rutin at doses of 50, 100 and 200 mg/kg significantly prevented the increase of gastric mucosal injury index induced by gastric I/R (73.4 AE 14.8, 65.9 AE 9.6 and 26.9 AE 5.7, respectively). ED 50 value was 138.7 mg/kg. Moreover, rutin at doses of 50, 100 and 200 mg/kg showed an inhibition on the increased myeloperoxidase (24.6, 41.3 and 53.1% reduction) activity and malondialdehyde levels (27.4, 40.3 and 50.7% reduction) in gastric mucosa. Also, the elevation of inducible NO synthase (iNOS) activity as well as the decrease of constitutive NO synthase (cNOS) in the gastric mucosa were significantly prevented by rutin pretreatment. Conclusion: These results suggested that rutin has a protective effect against gastric mucosal injury induced by gastric I/R and that the gastroprotection was related to the NOS/NO pathway and its antioxidant activity.

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Protective Effect of Acetaminophen against Acute Gastric Mucosal Lesions Induced by Ischemia-Reperf usion in the Rat

Cited by 21 publications

References 23 publications

Effects ofL-carnitine on neutrophil-mediated ischemia–reperfusion injury in rat stomach

Effects ofL-carnitine on neutrophil-mediated ischemia–reperfusion injury in rat stomach

Acetaminophen and low-flow myocardial ischemia: efficacy and antioxidant mechanisms

Protective effect of rutin against acute gastric mucosal lesions induced by ischemia-reperfusion

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