Influence of Intestinal Strangulation Release on Ischemiareperfusion Injury in Sprague Dawley Rats

Background: In intestinal ischemia, reperfusion towards the injured intestine can cause further injury to the intestine itself and to remote organs. This research aimed to evaluate the influence of intestinal strangulation release (SR) before resection on the intestine outside margin of the strangulated intestine compared with subjects without intestinal strangulation release (WSR). Methods: Fourteen male Sprague Dawley rats were subjected to strangulation of one loop of the distal ileum for 4 h. In the SR group, the strangulated intestine was released for 5 min and then resected for necrotic parts. In the WSR group, the strangulated intestine was immediately resected WSR. The control group received a sham laparotomy. Four hours after the second laparotomy, the animals weresacrificed, and intestinal samples were taken for histomorphological analysis and measurement of intestinal malondialdehyde (MDA) level. Results: The injury on the histomorphological intestinal mucosa and intestinal MDA level were insignificantly higher in the SR group than in the WSR group (p>0.05). Conclusion: Intestinal SR before resection causes more tissue injury and oxidative stress on the intestine outside the strangulationsection, but the difference is not statistically significant. Keywords: Ischemia-reperfusion injury, Intestinal ischemia, Intestinal strangulation release, Malondialdehyde, Intestine injury

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Prophylactic Ozone Administration Reduces Intestinal Mucosa Injury Induced by Intestinal Ischemia-Reperfusion in the Rat

Mediators of Inflammation ◽

10.1155/2015/792016 ◽

2015 ◽

Vol 2015 ◽

pp. 1-8 ◽

Cited By ~ 10

Author(s):

Ozkan Onal ◽

Fahri Yetisir ◽

A. Ebru Salman Sarer ◽

N. Dilara Zeybek ◽

C. Oztug Onal ◽

...

Keyword(s):

Reperfusion Injury ◽

Intestinal Ischemia ◽

Ischemia Reperfusion Injury ◽

Tissue Injury ◽

Ischemia Reperfusion ◽

Intestinal Injury ◽

Control Group ◽

Injury Score ◽

Tissue Samples ◽

Intestinal Ischemia Reperfusion

Objectives. Intestinal ischemia-reperfusion injury is associated with mucosal damage and has a high rate of mortality. Various beneficial effects of ozone have been shown. The aim of the present study was to show the effects of ozone in ischemia reperfusion model in intestine.Material and Method. Twenty eight Wistar rats were randomized into four groups with seven rats in each group. Control group was administered serum physiologic (SF) intraperitoneally (ip) for five days. Ozone group was administered 1 mg/kg ozone ip for five days. Ischemia Reperfusion (IR) group underwent superior mesenteric artery occlusion for one hour and then reperfusion for two hours. Ozone + IR group was administered 1 mg/kg ozone ip for five days and at sixth day IR model was applied. Rats were anesthetized with ketamine∖xyzlazine and their intracardiac blood was drawn completely and they were sacrificed. Intestinal tissue samples were examined under light microscope. Levels of superoxide dismutase (SOD), catalase (CAT), glutathioneperoxidase (GSH-Px), malondyaldehide (MDA), and protein carbonyl (PCO) were analyzed in tissue samples. Total oxidant status (TOS), and total antioxidant capacity (TAC) were analyzed in blood samples. Data were evaluated statistically by Kruskal Wallis test.Results. In the ozone administered group, degree of intestinal injury was not different from the control group. IR caused an increase in intestinal injury score. The intestinal epithelium maintained its integrity and decrease in intestinal injury score was detected in Ozone + IR group. SOD, GSH-Px, and CAT values were high in ozone group and low in IR. TOS parameter was highest in the IR group and the TAC parameter was highest in the ozone group and lowest in the IR group.Conclusion. In the present study, IR model caused an increase in intestinal injury.In the present study, ozone administration had an effect improving IR associated tissue injury. In the present study, ozone therapy prevented intestine from ischemia reperfusion injury. It is thought that the therapeutic effect of ozone is associated with increase in antioxidant enzymes and protection of cells from oxidation and inflammation.

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Intravenous Administration of Tetramethylpyrazine Reduces Intestinal Ischemia-Reperfusion Injury in Rats

The American Journal of Chinese Medicine ◽

10.1142/s0192415x13500559 ◽

2013 ◽

Vol 41 (04) ◽

pp. 817-829 ◽

Cited By ~ 8

Author(s):

Štefan Tóth ◽

Tímea Pekárová ◽

Ján Varga ◽

Štefan Tóth ◽

Vladimíra Tomečková ◽

...

Keyword(s):

Reperfusion Injury ◽

Intestinal Ischemia ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Medical Intervention ◽

Biologically Active ◽

Pharmacological Intervention ◽

Control Group ◽

Therapeutic Effects ◽

Intestinal Ischemia Reperfusion

Intestinal ischemia-reperfusion injury (IIRI) is a life-threatening condition requiring prompt medical intervention. Tetramethylpyrazine (TMP) is a biologically active alkaloid isolated from Ligusticum wallichii. Previously, it was shown that TMP causes vasodilatation and inhibition of platelet aggregation as well as exhibits significant antioxidant effects. Therefore, the aim of the present study was to evaluate possible therapeutic effects of TMP in the prevention of IIRI. Wistar rats (n = 80) were randomly divided into eight experimental groups and subjected to a 1 h occlusion of cranial mesenteric artery followed by 0, 1, 12, and 24 h period of reperfusion. Thirty minutes before the IIRI animals received either TMP (30 mg/kg, i.v.) or identical volume of saline. In addition, a control group of 10 animals was not exposed to IIRI. Intestine morphology was evaluated by using histopathological injury index examination (HII), goblet and Paneth cells quantification as well as by applying immunofluorescent methods such as InSitu TUNEL and caspase-3 positivity assessment. Here we showed that preconditioning with TMP prior IIRI decreases the grade of injury. Significant reduction of HII was detected in TMP pretreated groups after 0, 1, and 12 h of reperfusion where injury reduction up to 75% was found. Lower histopathological damage in preconditioned groups was accompanied with increased number of secretory epithelial cells and decreased number of apoptotic cells. These results demonstrate the protective effect of TMP on the small intestine mucosa, suggesting administration of TMP as a molecule for pharmacological intervention against IIRI.

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Glycine Protects the Liver from Reperfusion Injury following Pneumoperitoneum

European Surgical Research ◽

10.1159/000490309 ◽

2018 ◽

Vol 59 (1-2) ◽

pp. 91-99 ◽

Cited By ~ 2

Author(s):

Mohammed Al-Saeedi ◽

Arash Nickkholgh ◽

Daniel Schultze ◽

Christa Flechtenmacher ◽

Markus Zorn ◽

...

Keyword(s):

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Control Group ◽

Sprague Dawley ◽

Co2 Pneumoperitoneum ◽

Hepatic Microcirculation ◽

Exact Test ◽

Sprague Dawley Rats ◽

Latex Beads

Background: Experimental pneumoperitoneum induces ischemia/reperfusion injury (IRI) in the liver, most likely via Kupffer cell (KC)-dependent mechanisms. Glycine has been shown to ameliorate IRI in various animal models. Thus, this study was performed to assess the effects of glycine on the liver after pneumoperitoneum. Materials and Methods: Sprague-Dawley rats (220–250 g in weight) underwent CO2 pneumoperitoneum (12 mm Hg) for 90 min. Some rats received i.v. glycine (1.5 mL, 300 mM) 10 min before pneumoperitoneum. Controls were given the same volume of Ringer’s solution. Transaminases, hepatic microcirculation, and phagocytosis of latex beads indexing both liver injury and KC activation were examined following pneumoperitoneum. Analysis of variance (ANOVA), plus a subsequent t test or χ2 test (or Fisher’s exact test) were carried out as appropriate. Results are presented as mean ± SEM. Results: Glycine significantly decreased lactate dehydrogenase at 1 h and both aspartate aminotransferase and alanine aminotransferase at 2 h after pneumoperitoneum from 477 ± 43, 154 ± 17, and 60 ± 6 U/L in controls to 348 ± 25, 101 ± 11, and 34 ± 3 U/L, respectively (p < 0.05). In parallel, glycine significantly decreased both the rate of permanent adherence of leukocytes to the endothelium by up to 35% and the rate of phagocytosis by > 50% compared to the control group. Conclusion: Glycine decreased IRI after pneumoperitoneum, most likely via KC-dependent mechanisms.

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The Mechanism of Sevoflurane Preconditioning-Induced Protections against Small Intestinal Ischemia Reperfusion Injury Is Independent of Mast Cell in Rats

Mediators of Inflammation ◽

10.1155/2013/378703 ◽

2013 ◽

Vol 2013 ◽

pp. 1-12 ◽

Cited By ~ 13

Author(s):

Xiaoliang Gan ◽

Guangjie Su ◽

Weicheng Zhao ◽

Pinjie Huang ◽

Gangjian Luo ◽

...

Keyword(s):

Mast Cell ◽

Intestinal Ischemia ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Artery Occlusion ◽

Intestinal Injury ◽

Sprague Dawley ◽

Sevoflurane Preconditioning ◽

Small Intestinal ◽

Intestinal Ischemia Reperfusion

The study aimed to investigate whether sevoflurane preconditioning can protect against small intestinal ischemia reperfusion (IIR) injury and to explore whether mast cell (MC) is involved in the protections provided by sevoflurane preconditioning. Sprague-Dawley rats exposed to sevoflurane or treated with MC stabilizer cromolyn sodium (CS) were subjected to 75-minute superior mesenteric artery occlusion followed by 2-hour reperfusion in the presence or absence of MC degranulator compound 48/80 (CP). Small intestinal ischemia reperfusion resulted in severe intestinal injury as demonstrated by significant elevations in intestinal injury scores and p47phoxand gp91phox, ICAM-1 protein expressions and malondialdehyde and IL-6 contents, and MPO activities as well as significant reductions in SOD activities, accompanied with concomitant increases in mast cell degranulation evidenced by significant increases in MC counts, tryptase expression, andβ-hexosaminidase concentrations, and those alterations were further upregulated in the presence of CP. Sevoflurane preconditioning dramatically attenuated the previous IIR-induced alterations except MC counts, tryptase, andβ-hexosaminidase which were significantly reduced by CS treatment. Furthermore, CP exacerbated IIR injury was abrogated by CS but not by sevoflurane preconditioning. The data collectively indicate that sevoflurane preconditioning confers protections against IIR injury, and MC is not involved in the protective process.

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