Mesenteric Lymphadenectomy Prevents Postburn Systemic Spread of Translocated Bacteria

Tokyay, Rifat; Zeigler, Stephen T.; Loick, H. M.; Heggers, John P.; Garza, Paul De la; Traber, Daniel L.; Herndon, David N.

doi:10.1001/archsurg.1992.01420040026003

Cited by 22 publications

(12 citation statements)

References 31 publications

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“…Based on previous studies, it is clear that the lymphatic route is the major route of BT [19]. As seen in our study, the MLN have the highest incidence of translocation.…”

Section: Resultssupporting

confidence: 77%

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 Blood was not withdrawn from sham rats.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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“…Based on previous studies, it is clear that the lymphatic route is the major route of BT [19]. As seen in our study, the MLN have the highest incidence of translocation.…”

Section: Resultssupporting

confidence: 77%

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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“…Gut mucosal injury as a consequence of both post-hemorrhagic perfusion impairment and pulmonary infection might cause bacterial translocation [17][18][19]. Bacterial translocation is defined as the passage of viable bacteria from the gastrointestinal tract through the mucosal epithelium to other sites, such as the MLNs, and may lead to the development of immune dysfunction [multiple organ dysfunctions (MODs)] after hemorrhagic shock [20].…”

Section: Discussionmentioning

confidence: 99%

The Effect of Hypothermia on Splanchnic Flows and Lung in a Two-Hit Hemorrhagic Shock Model

Deniz¹,

Ağalar²,

Agalar³

et al. 2010

Journal of Surgical Research

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“…This fact might explain the difference in NOS 2 expression between pigs and rodents during endotoxemia. Moreover, bacterial translocation that might occur during endotoxemia was more likely to reach the systemic circulation through the mesenteric lymph node than through the portal vein (22,34).…”

Section: Discussionmentioning

confidence: 99%

Minor involvement of nitric oxide during chronic endotoxemia in anesthetized pigs

Pastor¹,

Hadengue²,

Nüssler³

2000

American Journal of Physiology-Gastrointestinal and Liver Physi

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Pastor, Catherine M., Antoine Hadengue, and Andreas K. Nussler. Minor involvement of nitric oxide during chronic endotoxemia in anesthetized pigs. Am. J. Physiol. Gastrointest. Liver Physiol. 278: G416-G424, 2000.-To study the modifications of hepatic blood flow and hepatic function over time during endotoxemia, 10 pigs received a continuous intravenous infusion of endotoxin (Endo, 160 ng · kg Ϫ1 ·h Ϫ1 ) over 18 h and 7 control (Ctrl) animals received a saline infusion. The involvement of nitric oxide (NO) in this endotoxic model was assessed by measuring plasma concentrations of NO 2 Ϫ , NO 3 Ϫ , and cGMP, by testing vascular reactivity to ACh, and by evaluating inducible NO synthase (NOS 2) expression in hepatic biopsies. Endotoxin induced hypotensive and normokinetic shock in association with few modifications of hepatic blood flow, and hepatic injury was observed in both groups. Endotoxin did not increase plasma concentrations of NO 2 Ϫ , NO 3 Ϫ , and cGMP. The ACh-dependent decrease of mean arterial pressure was reduced in Endo pigs, whereas a minor difference was observed between Ctrl and Endo pigs for ACh-dependent modification of hepatic perfusion. Hepatic NOS 2 mRNA was not detected in Ctrl pigs. In Endo pigs, NOS 2 protein expression was detected only in tissues surrounding the portal vein and the inferior vena cava, whereas NOS 2 mRNA was expressed in all hepatic biopsies. Thus, although endotoxemia induces NOS 2 expression in the liver, our findings show that NO involvement is lower in pigs than in rodents during endotoxemia. liver; vascular reactivity; acetylcholine; inducible nitric oxide synthase; hepatic circulation SEPTIC SHOCK, which remains an important cause of death in intensive care units, is characterized by hypotension, vascular hyporeactivity to vasoactive agents, myocardial dysfunction, and altered regional blood flows (4, 25). The multiple-organ dysfunction syndrome, which is defined as two or more organs failing at the same time, frequently occurs and is associated with a high mortality rate. Endotoxin, which is included in the wall of Gram-negative bacteria, is responsible for most of the abnormalities observed in sepsis and is commonly used to mimic septic shock in experimental models.The liver is crucial in severe sepsis because it contains most of the macrophages of the body (Kupffer cells) able to clear endotoxin and bacteria that may stimulate the systemic inflammatory response. Moreover, hepatocytes synthesize the acute-phase proteins and enzymes necessary to modulate the inflammatory response. Finally, because hepatic blood flow represents 25% of cardiac output (CO), modifications of hepatic perfusion may greatly interfere with systemic hemodynamics.Nitric oxide (NO) is one of the major mediators that induce cardiovascular abnormalities during septic shock. Under physiological conditions, the constitutive endothelial isoform of NO synthase (eNOS or NOS 3) produces low levels of NO and regulates vascular tone as well as numerous cell functions (24). In contrast, during sepsis,...

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Mesenteric Lymphadenectomy Prevents Postburn Systemic Spread of Translocated Bacteria

Cited by 22 publications

References 31 publications

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

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

The Effect of Hypothermia on Splanchnic Flows and Lung in a Two-Hit Hemorrhagic Shock Model

Minor involvement of nitric oxide during chronic endotoxemia in anesthetized pigs

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