Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/7041
Title: Effects of Tempol, a Membrane-Permeable Radical Scavenger, on Local and Remote Organ Injuries Caused by Intestinal Ischemia/Reperfusion in Rats
Authors: Teke, Z.
Kabay, Burhan
Özden, Akın
Yenisey, C.
Bir, Ferda
Demirkan, N.C.
Bicakci, T.
Keywords: acute lung injury
glutathione
intestinal mucosal injury
ischemia/reperfusion
malondialdehyde
mesenteric ischemia
myeloperoxidase
neutrophil
nitrate
nitrite
pulmonary microvascular dysfunction
reperfusion injury
Tempol
Evans blue
malonaldehyde
scavenger
tempol
animal experiment
animal model
animal tissue
article
controlled study
drug mechanism
histopathology
intestine injury
intestine ischemia
intestine mucosa
laparotomy
lung injury
lung parenchyma
male
membrane permeability
neutrophil chemotaxis
nonhuman
priority journal
rat
superior mesenteric artery obstruction
Animals
Capillary Permeability
Cyclic N-Oxides
Edema
Free Radical Scavengers
Glutathione
Intestinal Mucosa
Lung
Male
Malondialdehyde
Mesenteric Artery, Superior
Mesenteric Vascular Occlusion
Neutrophils
Nitrates
Nitrites
Peroxidase
Rats
Rats, Wistar
Reperfusion Injury
Respiratory Distress Syndrome, Adult
Spin Labels
Abstract: Background: Tempol is a stable piperidine nitroxide of low molecular weight that permeates biological membranes and scavenges superoxide anions in vitro. In a variety of animal models, deleterious effects of reperfusion injury on both local and remote organs have been demonstrated. In this study, we aimed to investigate the effects of a membrane-permeable radical scavenger, Tempol, on local and remote organ injuries caused by intestinal ischemia/reperfusion (I/R) in rats. Materials and methods: Male Wistar-albino rats were randomized into three groups: (I) Sham-operated control group, laparotomy without I/R injury (n = 12); (II) Intestinal I/R group, 60 min of ischemia by superior mesenteric artery occlusion followed by 2-h of reperfusion (n = 12); and (III) I/R + Tempol-treated group, identical to I/R group except for Tempol administration, 30 mg/kg bolus injection 5 min before reperfusion, followed by an infusion of 30 mg/kg/h intravenously (n = 12). Histopathologically, intestinal mucosal lesions were assessed by Chiu's classification, and pulmonary parenchymal damage was appraised by pulmonary neutrophil infiltration and acute lung injury scaling. Biochemically, myeloperoxidase activity, malondialdehyde, glutathione, and nitrite/nitrate (NOx) levels were determined in both intestinal mucosa and lung parenchyma. Evans blue dye concentration and organ wet/dry weight ratios were used as a marker of organ edema. Animal survival was observed up to 1 week. Results: Intestinal mucosal lesions and pulmonary parenchymal damage were significantly attenuated with Tempol treatment, histopathologically (P < 0.05). Tempol administration significantly reduced myeloperoxidase activity and malondialdehyde levels, and also significantly increased glutathione and NOx levels of both intestinal and lung tissues, biochemically (P < 0.05). Evans blue dye extravasation and wet/dry weight ratios of organs were significantly reduced with Tempol injection (P < 0.05). The survival rates of rats in Tempol-treated group were significantly higher than that of I/R-treated group (P < 0.05). Conclusions: The present study suggests that Tempol administration significantly reduces both local and remote organ injuries caused by intestinal I/R before and throughout the reperfusion period. Further clinical studies are needed to clarify whether Tempol may be a useful therapeutic agent to use in particular operations where the reperfusion injury occurs. © 2008 Elsevier Inc. All rights reserved.
URI: https://hdl.handle.net/11499/7041
https://doi.org/10.1016/j.jss.2007.12.791
ISSN: 0022-4804
Appears in Collections:PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tıp Fakültesi Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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