Translocation of 99mTc labelled bacteria after intestinal ischemia and reperfusion

João, Samir Assi; Alencar, Suelene Suassuna Silvestre de; Medeiros, Aldo da Cunha; Diniz, S.A.; Cardoso, Valbert Nascimento; Brandt, Carlos Teixeira

doi:10.1590/s0102-86502004000400003

Cited by 15 publications

(13 citation statements)

References 15 publications

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“…All the organs from rats observed for 24 h after reperfusion had signifi cantly higher levels of radioactivity and positive cultures than did the organs of rats reperfused for 30 min, sham and controls, except in the spleen indicating that intestinal ischaemia/reperfusion led to bacterial translocation, mostly after 24 h of reperfusion. This method has the advantage that even if bacteria are killed by gut associated lymphoid tissue when they traverse the intestinal epithelial barrier [47] they can still be located.…”

Section: Measurement Of Bacterial Translocationmentioning

confidence: 99%

Translocation of gut flora and its role in sepsis

Vaishnavi

2013

Indian Journal of Medical Microbiology

140

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Bacterial translocation is the invasion of indigenous intestinal bacteria through the gut mucosa to normally sterile tissues and the internal organs. Sometimes instead of bacteria, inflammatory compounds are responsible for clinical symptoms as in systemic inflammatory response syndrome (SIRS). The difference between sepsis and SIRS is that pathogenic bacteria are isolated from patients with sepsis but not with those of SIRS. Bacterial translocation occurs more frequently in patients with intestinal obstruction and in immunocompromised patients and is the cause of subsequent sepsis. Factors that can trigger bacterial translocation from the gut are host immune deficiencies and immunosuppression, disturbances in normal ecological balance of gut, mucosal barrier permeability, obstructive jaundice, stress, etc. Bacterial translocation occurs through the transcellular and the paracellular pathways and can be measured both directly by culture of mesenteric lymph nodes and indirectly by using labeled bacteria, peripheral blood culture, detection of microbial DNA or endotoxin and urinary excretion of non-metabolisable sugars. Bacterial translocation may be a normal phenomenon occurring on frequent basis in healthy individuals without any deleterious consequences. But when the immune system is challenged extensively, it breaks down and results in septic complications at different sites away from the main focus. The factors released from the gut and carried in the mesenteric lymphatics but not in the portal blood are enough to cause multi-organ failure. Thus, bacterial translocation may be a promoter of sepsis but not the initiator. This paper reviews literature on the translocation of gut flora and its role in causing sepsis.

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Section: Measurement Of Bacterial Translocationmentioning

confidence: 99%

Translocation of gut flora and its role in sepsis

Vaishnavi

2013

Indian Journal of Medical Microbiology

140

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“…Occlusion and reperfusion of the splanchnic arteries cause circulatory shock, especially due to an increase in vascular permeability, activation and adherence of polymorphonuclear neutrophils, release of proinflammatory substances, formation of reactive oxygen species (ROS) and reactive nitrogen species 4,5 . Mucosal injury, bacterial translocation and activation of inflammatory responses occur in the small intestine 6 , besides hydroelectrolytic disorders and acid-base imbalance in remote organs 7 . Splanchnic artery occlusion shock (SAO shock) is an experimental type of circulatory shock that results from ischemia and reperfusion of the splanchnic region.…”

Section: Introductionmentioning

confidence: 99%

Systemic evaluation on ischemia and reperfusion injury of splanchnic organs in rats

Cerqueira¹,

Hussni

Yoshida

et al. 2009

Acta Cir. Bras.

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Purpose:To evaluate hemodynamic and systemic changes during and after splanchnic ischemia and reperfusion (I/R). Methods: Rats were divided into two groups: a) control: animals submitted to surgery, but not to I/R, treated with saline (5 ml/kg/h) for 150 min; b) group I/R: animals continuously infused with saline, and submitted to occlusion of the celiac trunk, superior mesenteric artery (SMA), and inferior mesenteric artery for 30 min, followed by a 120-min reperfusion. Mean arterial blood pressure (MABP), venous pressure, aortic and SMA blood flow, heart rate, esophageal temperature and hematocrit were evaluated. Results: During reperfusion in I/R groups, there was a progressive decrease in MABP, aortic blood flow, SMA blood flow, heart rate and esophageal temperature; vein pressure and hematocrit remained unchanged during the experiment. Conclusion: The model of ischemia used causes systemic changes, which are evidenced by hypotension, decrease in mesenteric blood flow, heart rate and esophageal temperature. Key words: Ischemia. Reperfusion. Intestine, Small. Shock. Rats. RESUMOObjetivo: Avaliar as alterações hemodinâmicas e sistêmicas decorrentes de isquemia e reperfusão (I/R) esplâncnica em ratos. Métodos: Vinte ratos foram divididos em dois grupos: grupo controle: os animais foram submetidos à cirurgia, mas não a I/R e foram tratados com solução fisiológica (5 ml/kg/h) por 150 minutos; grupo I/R: os animais foram submetidos à administração contínua de solução fisiológica e à oclusão do tronco celíaco, artéria mesentérica superior e artéria mesentérica inferior por 30 minutos, seguidos por 120 minutos de reperfusão. Avaliou-se a pressão arterial média, pressão venosa, fluxo sangüíneo na aorta e na artéria mesentérica superior, freqüência cardíaca, temperatura esofágica e hematócrito. Resultados: Durante a reperfusão, no grupo I/R, houve uma diminuição progressiva da pressão arterial média, fluxo sangüíneo na aorta e artéria mesentérica superior, freqüência cardíaca e temperatura esofágica; pressão venosa e hematócrito não sofreram alteração. Conclusão: O modelo de isquemia provocado por oclusão da artéria mesentérica superior, artéria mesentérica inferior e tronco celíaco por 30 minutos seguidos por 120 minutos de reperfusão provoca alterações sistêmicas evidenciadas por hipotensão, diminuição do fluxo sangüíneo mesentérico, da freqüência cardíaca e da temperatura esofágica. Descritores: Isquemia. Reperfusão. Intestino Delgado. Choque. Ratos.

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“…I/R can provoke complex interactions between the endothelium and different cell types, leading to microvascular injury, cellular necrosis and/or apoptosis (Massberg & Messmer, 1998). Ischemia and reperfusion of the small intestine provoke the rupture of the mucosa barrier, bacterial translocation and the activation of inflammatory responses (João et al, 2004). Histological damage that occurs after intestinal I/R in the form of shortening of the villi length, loss of villus epithelium, dilatation and congestion of blood vessels, degeneration of epithelial cells with nuclear alterations and invasion by inflammatory cells were coincided with the results of the present work (Tunc et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Effects of Potentilla Fulgens as Prophylactic Agent in Intestinal Ischemia Reperfusion Injury

et al. 2015

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SUMMARY:The purpose of this study, ischemia reperfusion injury in rats, Potentilla fulgens is to investigate the protective effects. Wistar albino rats (n= 30) weighing 180-220 g were used in the experiment. Group 1 animals underwent sham laparotomy without ischemiareperfusion injury. Group 2 animals underwent laparotomy and occlusion of superior mesenteric arteries for 30 min followed by 20 min of reperfusion without pretreatment. The Potentilla fulgens group received 400 mg/kg/day Potentilla fulgens intraperitoneally 5 days before Ischemia-reperfusion injury. There was a significant difference between the group with ischemia-reperfusion group Potentilla fulgens (p<0.0001). In statistical analysis of the MDA level, data were obtained after a respective measurement in all groups. Potentilla fulgens group with ischemia-reperfusion group was a significant decrease in MDA (p<0.001). In the period after ischemia-reperfusion, marked PCNA immunoreactivities were observed in the nuclei of crypt and villus cell. In ischemia reperfusion group, the number of PCNA immunoreactivity is quite advanced and they extended throughout the middle part of the intestine folds. The number of TUNEL-positive nuclei were also developed. In ischemia-reperfusion plus P. fulgens group, the intestinal epithelium with only a few PCNA immunoreactive nuclei. TUNEL positive nuclei were noted in the gut lumen and mucosal close differentiated goblet cells. We showed that Potentilla fulgens extract significantly prevented mucosal lesions caused by intestinal ıschemia-reperfusion.

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Translocation of 99mTc labelled bacteria after intestinal ischemia and reperfusion

Cited by 15 publications

References 15 publications

Translocation of gut flora and its role in sepsis

Translocation of gut flora and its role in sepsis

Systemic evaluation on ischemia and reperfusion injury of splanchnic organs in rats

Effects of Potentilla Fulgens as Prophylactic Agent in Intestinal Ischemia Reperfusion Injury

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