scholarly journals Translocation of 99mTc labelled bacteria after intestinal ischemia and reperfusion

2004 ◽  
Vol 19 (4) ◽  
pp. 328-333 ◽  
Author(s):  
Samir Assi João ◽  
Suelene Suassuna Silvestre de Alencar ◽  
Aldo da Cunha Medeiros ◽  
Simone Otília Fernandes Diniz ◽  
Valbert Nascimento Cardoso ◽  
...  
Keyword(s):  
Bacterial Translocation ◽  
Intestinal Ischemia ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Ischemia And Reperfusion ◽  
Mesenteric Lymph Nodes ◽  
Mesenteric Lymph ◽  
Colony Forming Units ◽  
Male Wistar Rats ◽  
Intestinal Ischemia Reperfusion

PURPOSE: Ischemia and reperfusion of the small intestine disrupts gut barrier, causes bacterial translocation and activates inflammatory responses. An experimental study was planned to evaluate if 99mTc labelled Escherichia coli translocates to mesenteric lymph nodes, liver, spleen, lung and serum of rats submitted to mesenteric ischemia/reperfusion. Additionally, it was observed if the time of reperfusion influences the level of translocation. METHODS: Forty male Wistar rats underwent 45 minutes of gut ischemia by occlusion of the superior mesenteric artery. The translocation of labelled bacteria to different organs and portal serum was determined in rats reperfused for 30 minutes, 24 hours, sham(S) and controls(C), using radioactivity count and colony forming units/g (CFU). RESULTS: All the organs from rats observed for 24 hours after reperfusion had higher levels of radioactivity and positive cultures (CFU) than did the organs of rats reperfused for 30 minutes, C and S, except in the spleen (p<0,01). CONCLUSION: The results of this study indicated that intestinal ischemia/reperfusion led to bacterial translocation, mostly after 24 hours of reperfusion.

scholarly journals Prevention of bacterial translocation using beta-(1-3)-D-glucan in small bowel ischemia and reperfusion in rats

2006 ◽  
Vol 21 (suppl 4) ◽  
pp. 18-22 ◽  
Author(s):  
Irami Araújo-Filho ◽  
Amália Cínthia Meneses Rêgo ◽  
Laíza Araújo Mohana Pinheiro ◽  
Italo Medeiros Azevedo ◽  
Vítor Brasil Medeiros ◽  
...  
Keyword(s):  
Small Bowel ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Bowel Ischemia ◽  
Ischemia And Reperfusion ◽  
Mesenteric Lymph Nodes ◽  
Mesenteric Lymph ◽  
Group I ◽  
Colony Forming Units

PURPOSE: To investigate the role of beta-(1-3)-D-glucan on 99mTc labelled Escherichia coli translocation and cytokines secretion in rats submitted to small bowel ischemia/reperfusion injury. METHODS: Five groups (n=10 each) of Wistar rats were subjected to control(C), sham(S), group IR subjected to 45 min of bowel ischemia/60 min of reperfusion(I/R), and group I/R+glucan subjected to 45 min of bowel ischemia/60 min of reperfusion(I/R) and injected with 2mg/Kg intramuscular. Translocation of labelled bacteria to mesenteric lymph nodes, liver, spleen, lung and serum was determined using radioactivity/count and colony forming units/g(CFU/g). Serum TNFalpha, IL-1beta, IL-6, IL-10 were measured by ELISA. RESULTS: CFU/g and radioactivity/count were higher in I/R than in I/R+glucan rats. In C, S and S+glucan groups, bacteria and radioactivity/count were rarely detected. The I/R+glucan rats had enhancement of IL-10 and suppressed production of serum TNFalpha, IL-1beta and, IL-6, compared to I/R untreated animals. CONCLUSION: The beta-(1-3)-D-glucan modulated the production of pro-inflammatory and anti-inflammatory cytokines during bowel ischemia/reperfusion, and attenuated translocation of labelled bacteria.

Mucosal arachidonate metabolism and intestinal ischemia-reperfusion injury

1989 ◽  
Vol 257 (2) ◽  
pp. G299-G307 ◽  
Author(s):  
M. J. Mangino ◽  
C. B. Anderson ◽  
M. K. Murphy ◽  
E. Brunt ◽  
J. Turk
Keyword(s):  
Blood Flow ◽  
Reperfusion Injury ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Leukotriene B4 ◽  
Time Dependent ◽  
Ischemia And Reperfusion ◽  
Synthesis Inhibitor ◽  
Intestinal Ischemia Reperfusion

Mucosal arachidonic acid metabolism was examined after 3 h of ischemia and 1 h of reperfusion in isolated ileal segments in the dog. The cyclooxygenase products thromboxane B2, 6-ketoprostaglandin F1 alpha, and prostaglandin E2 increased by 365%, 97%, and 158%, respectively, after ischemia and reperfusion but were not altered after 3 h of ischemia alone. The potent chemotactic lipoxygenase product leukotriene B4 (LTB4) increased by 687% after ischemia and reperfusion and was not affected by ischemia without reperfusion. In addition, tissue production of the thiol ether leukotrienes (LTC4, LTD4, and LTE4) increased threefold after ischemia and reperfusion. Quantitation of regionally isomeric hydroxy acids produced from arachidonate revealed a 300% increase in 12-hydroxyeicosatetraenoate (12-HETE) after intestinal ischemia and reperfusion without a change in other isomers (15-HETE and 5-HETE). Stereochemical analysis of 12-HETE demonstrated exclusive synthesis of the S-enantiomer. A significant and time-dependent decrease in intestinal blood flow also occurred during reperfusion. Administration of the dual cyclooxygenase-lipoxygenase synthesis inhibitor BW755C (1 mg/kg ia) did not alter time-dependent decreases in blood flow and failed to inhibit eicosanoid synthesis. Histologic examinations of intestinal samples revealed significant mucosal damage associated with ischemia alone and ischemia after reperfusion. This study indicates that intestinal ischemia-reperfusion injury is associated with dramatic alterations in mucosal production of vasoactive eicosanoids and with changes in blood flow that occur during reperfusion but not during ischemia alone. These events may be involved in the pathology characteristic of this injury.

Intestinal ischemia and reperfusion injury in transgenic mice overexpressing copper-zinc superoxide dismutase

1997 ◽  
Vol 273 (4) ◽  
pp. C1130-C1135 ◽  
Author(s):  
Devendra R. Deshmukh ◽  
Oleg Mirochnitchenko ◽  
Vikram S. Ghole ◽  
Doreen Agnese ◽  
Pritesh C. Shah ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Transgenic Mice ◽  
Reperfusion Injury ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Neutrophil Infiltration ◽  
Myeloperoxidase Activity ◽  
Ischemia And Reperfusion ◽  
Intestinal Ischemia Reperfusion

Superoxide dismutase (SOD) scavenges oxygen radicals that are implicated in the pathogenesis of intestinal ischemia-reperfusion injury. The effect of intestinal ischemia and reperfusion was investigated in transgenic mice overexpressing human Cu-Zn SOD. Ischemia was induced by occluding the superior mesenteric artery. Myeloperoxidase activity was determined as an index of neutrophil infiltration, and malondialdehyde levels were measured as an indicator of lipid peroxidation. Forty-five minutes of intestinal ischemia followed by 4 h of reperfusion caused an increase in intestinal levels of malondialdehyde in both nontransgenic and transgenic mice, but the concentration of malondialdehyde was significantly greater in nontransgenic mice. Intestinal ischemia-reperfusion also caused an increase in intestinal and pulmonary myeloperoxidase activity in nontransgenic and transgenic mice, but the transgenic mice had significantly lower levels of myeloperoxidase activity than nontransgenic mice. Transgenic mice had higher levels of intestinal SOD activity than nontransgenic mice. There were no significant differences in the catalase or glutathione peroxidase activities. In conclusion, our study demonstrates that the overexpression of SOD protects tissues from neutrophil infiltration and lipid peroxidation during intestinal ischemia-reperfusion.

scholarly journals Nicaraven Attenuates Postoperative Systemic Inflammatory Responses-Induced Tumor Metastasis

2019 ◽  
Vol 27 (4) ◽  
pp. 1068-1074 ◽  
Author(s):  
Xu Zhang ◽  
Takahito Moriwaki ◽  
Tsuyoshi Kawabata ◽  
Shinji Goto ◽  
Ke-Xiang Liu ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Tumor Metastasis ◽  
Intestinal Ischemia ◽  
Cancer Metastasis ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Inflammatory Cells ◽  
Major Surgery ◽  
Lewis Lung Cancer ◽  
Intestinal Ischemia Reperfusion

Abstract Background Inflammation has been demonstrated to promote cancer metastasis. Due to the well-known systemic inflammatory responses (SIR) after major surgery, it is critical to investigate and attenuate SIR-induced tumor metastasis of cancer patients suffering surgical procedures. Methods C57BL/6 mice were intravenously injected with Lewis lung cancer cells at 6, 24, and 72 h after the induction of intestinal ischemia/reperfusion (I/R) injury. We found that the number of tumor nodules significantly increased in lungs of mice injected with cancer cells at 6 h but not at 24 and 72 h after I/R injury. The administration of nicaraven 30 min before and 24 h after I/R injury effectively attenuated the enhanced tumor metastasis to lungs. Protein array showed the increase of various cytokines in plasma of mice at 6 h after I/R injury, but many of them were attenuated by the administration of nicaraven. Immunostaining indicated the increase of Ly6g-, CD206-, and CD11c-positive inflammatory cells in the lungs, but it was also attenuated by nicaraven administration. Conclusions Postoperative SIR-induced tumor metastasis have been clearly evidenced in our experimental model, and the administration of nicaraven may ameliorate the SIR-induced tumor metastasis by suppressing inflammatory responses.

Intestinal ischemia/reperfusion-induced bacterial translocation and lung injury in atherosclerotic rats with hypoadiponectinemia

Surgery ◽  
2009 ◽  
Vol 145 (1) ◽  
pp. 48-56 ◽  
Author(s):  
Hiromichi Nakagawa ◽  
Nobuo Tsunooka ◽  
Yuji Yamamoto ◽  
Motohira Yoshida ◽  
Tatsuhiro Nakata ◽  
...  
Keyword(s):  
Lung Injury ◽  
Bacterial Translocation ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion

Pitavastatin prevents intestinal ischemia/reperfusion–induced bacterial translocation and lung injury in atherosclerotic rats with hypoadiponectinemia

Surgery ◽  
2009 ◽  
Vol 145 (5) ◽  
pp. 542-549 ◽  
Author(s):  
Hiromichi Nakagawa ◽  
Nobuo Tsunooka ◽  
Yuji Yamamoto ◽  
Motohira Yoshida ◽  
Tatsuhiro Nakata ◽  
...  
Keyword(s):  
Lung Injury ◽  
Bacterial Translocation ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion

scholarly journals Protective effects of berberine on intestinal ischemia and reperfusion injury in rats

2017 ◽  
Vol 69 (1) ◽  
pp. 45-51 ◽  
Author(s):  
Tanzhou Chen ◽  
Bin Lv
Keyword(s):  
Reperfusion Injury ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Immunoglobulin A ◽  
Male Rats ◽  
Ischemia And Reperfusion ◽  
Protective Effects ◽  
Ischemia And Reperfusion Injury ◽  
Intestinal Ischemia Reperfusion

This study aims to investigate the potential protective effects of berberine on ischemia and reperfusion (IR) injury in rats. Thirty male rats were randomly divided into three experimental groups as follows: the sham group, the IR group and the berberine+IR group. Intestinal ischemia-reperfusion was performed by occlusion of the superior mesenteric artery for 30 min, followed by 2-h reperfusion. The berberine+IR group of rats were administered 200 mg/kg of berberine once a day for 7 days before laparotomy. Compared with the IR group, rats pretreated with berberine prior to IR had significantly reduced intestinal ischemia/reperfusion injury and a significant reduction in Chiu?s score (p<0.05). The level of malondialdehyde and myeloperoxidase in the berberine+IR group was significantly decreased compared with the IR group (p<0.001). Superoxide dismutase activity in the berberine+IR group was significantly higher than in the IR group (p<0.001). Compared with the IR group, diamine oxidase was markedly decreased in the berberine+IR group (p<0.01). The level of secretory immunoglobulin A in the berberine+IR group was significantly increased when compared to the IR group (p<0.001). Our results suggest that berberine can protect from intestinal IR injury and that it can be beneficial in treating conditions associated with intestinal IR injury.

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