Pentoxifylline improves bacterial clearance during hemorrhage and endotoxemia

Heller, Susanne; Weber, Kathrin; Heller, A. R.; Urbaschek, Renate; Koch, Thea

doi:10.1097/00003246-199904000-00031

Cited by 30 publications

(19 citation statements)

References 40 publications

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“…29 Animal studies have shown that PTX decreases bacterial translocation and tissue damage in a murine hemorrhage model 30 and significantly reduces lung and kidney bacterial colonization. 31 In a chronic endotoxemia model, PTX significantly reduced lung injury and ICAM-1 expression compared with LPS-treated animals. 32 PTX also downregulates PMN activation [33][34][35] and prevents endotoxin-induced PMN degranulation.…”

mentioning

confidence: 96%

LPS-Induced Acute Lung Injury is Attenuated by Phosphodiesterase Inhibition: Effects on Proinflammatory Mediators, Metalloproteinases, NF-??B, and ICAM-1 Expression

Coimbra

Melbostad

Loomis

et al. 2006

The Journal of Trauma: Injury, Infection, and Critical Care

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mentioning

confidence: 96%

LPS-Induced Acute Lung Injury is Attenuated by Phosphodiesterase Inhibition: Effects on Proinflammatory Mediators, Metalloproteinases, NF-??B, and ICAM-1 Expression

Coimbra

Melbostad

Loomis

et al. 2006

The Journal of Trauma: Injury, Infection, and Critical Care

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“…Pentoxifylline also inhibits the production of TNF- α by endotoxin-stimulated monocytes/macrophages at the transcriptional level and is effective in reducing serum TNF- α level in mice with endotoxic shock [40], so pentoxifylline as anti-TNF- α agent could decrease bacterial translocation as previously mentioned by Goldman and coworkers [28]. Heller and coworkers [41] have shown that pentoxifylline improves bacterial clearance during hemorrhage and endotoxemia and these authors suggested that pentoxifylline could reduce the risk of bacterial infections by attenuating bacterial colonization of organs. Further investigations showed that pentoxifylline potentially affects endotoxin-induced release of TNF- α which plays an important role in superantigen-mediated shock [18].…”

Section: Discussionmentioning

confidence: 99%

Role of Pentoxifylline and Sparfloxacin in Prophylaxis of Spontaneous Bacterial Peritonitis in Cirrhotic Patients

Mostafa

Ibrahim

Badra

et al. 2014

ISRN Gastroenterology

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This study was directed to evaluate the role of sparfloxacin and pentoxifylline in the prophylaxis of spontaneous bacterial peritonitis in cirrhotic patients. Forty cirrhotic patients with ascites were included in the study. Patients were randomized into four groups in a blind fashion; each group consists of ten patients. Group one received ciprofloxacin (control group), group two received sparfloxacin, group three received pentoxifylline, and group four received a combination of sparfloxacin and pentoxifylline. Treatment duration was six months. Serum TNF-α level was the primary inflammatory marker of the study to evaluate the effect of the used medications. In group two, TNF-α level showed a statistically significant decrease in comparison with group one (P = 0.001), while in group three, TNF-α level showed nonsignificant difference in comparison with the control group (P > 0.05). In addition, group four showed a statistically significant decrease in TNF-α level compared to the other three groups (P < 0.05). The finding from our study indicates that sparfloxacin as well as pentoxifylline could be used in prophylaxis of spontaneous bacterial peritonitis. Combination of sparfloxacin and pentoxifylline showed some of synergism which may be useful in decreasing emergence of resistant strains.

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“…This complex pathopysiology is likely to be multifactorial, involving improved host defense responses, decreased inflammatory cytokine release, enhanced cardiac output, organ perfusion, and organ function [25]. This beneficial effect of pentoxifylline may be due to the downregulation of tumor necrosis factor and interleukin-6 [26,27]. Moreover, it has been demonstrated that pentoxifylline inhibits the production of oxygen radicals, the release of lysosomal enzymes, and the formation of thromboxane A 2 .…”

Section: Discussionmentioning

confidence: 99%

“…By preventing the expression of adhesion molecules on the surface of polymorphonuclear granulocytes, reduced adherence on endothelial cells was shown after pentoxifylline [28,29]. An important pathomechanism in the progression of sepsis following hemorrhage is an impairment of the microcirculation resulting in hypoxic tissue injury [27]. Studies show that pentoxifylline treatment after hemorrhagic shock significantly improves tissue oxygenation and survival rate [9,25].…”

Section: Discussionmentioning

confidence: 99%

The effects of pentoxifylline treatment on bacterial translocation after hemorrhagic shock in rats

Köylüoğlu¹,

Bakıcı

Elagöz

et al. 2001

Clin Exp Med

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Bacterial translocation is thought to be responsible for infectious complications after hemorrhagic shock. The aim of this study was to investigate the effects of pentoxifylline treatment on bacterial translocation in animals subjected to hemorrhagic shock. Thirty-one Wistar albino rats (280-360 g) were divided into three groups: sham (n=10), shock (n=11), and shock-pentoxifylline (n=10). Blood was not withdrawn from sham rats. Shock rats were subjected to 30 min of shock followed by reinfusion of shed blood. Shock/pentoxifylline rats received pentoxifylline after reinfusion of shed blood. After hemorrhage and reinfusion (24 h), the mesenteric lymph nodes, liver, spleen, and blood samples were evaluated using quantitative microbiological techniques, and the numbers of colony-forming units were compared between groups. Cecum was removed to evaluate the bacterial population. Ileum and cecum were examined histologically. The incidence of bacterial translocation was higher in the shocked rats (63%) than in the sham shock rats (10%). Pentoxifylline reduced the incidence of shock-induced bacterial translocation to 0%. Cecal bacterial levels were significantly higher in the shock rats than in the sham and shock/pentoxifylline rats. The histological damage caused by hemorrhagic shock was prevented by pentoxifylline treatment. In conclusion, the hemorrhagic shock triggered translocation of bacteria to the mesenteric lymph nodes, spleen, liver, and blood of rats. Pentoxifylline treatment just after shed blood transfusion significantly attenuated this phenomenon.

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Pentoxifylline improves bacterial clearance during hemorrhage and endotoxemia

Abstract: Hemorrhage and endotoxemia induce impaired bacterial clearance from blood and tissue. Treatment with PTX may reduce the risk of bacterial infections by attenuating bacterial colonization of organs in states of hemorrhage and endotoxemia.

Cited by 30 publications

References 40 publications

LPS-Induced Acute Lung Injury is Attenuated by Phosphodiesterase Inhibition: Effects on Proinflammatory Mediators, Metalloproteinases, NF-??B, and ICAM-1 Expression

LPS-Induced Acute Lung Injury is Attenuated by Phosphodiesterase Inhibition: Effects on Proinflammatory Mediators, Metalloproteinases, NF-??B, and ICAM-1 Expression

Role of Pentoxifylline and Sparfloxacin in Prophylaxis of Spontaneous Bacterial Peritonitis in Cirrhotic Patients

The effects of pentoxifylline treatment on bacterial translocation after hemorrhagic shock in rats

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