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Plasma Endotoxin (plasma + endotoxin)

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Medical Sciences100%

Terms modified by Plasma Endotoxin

  • plasma endotoxin level
    		•

    Selected Abstracts

    Effect of Acute Ethanol Administration on the Intestinal Absorption of Endotoxin in Rats

    ALCOHOLISM, Issue 3 2000
    Hironao Tamai
    Background: Endotoxin has been implicated in the pathogenesis and progression of alcoholic liver disease. Not only inactivation of reticuloendothelial function, which reduces clearance of endotoxin, but also an increase in absorption of endotoxin from the intestine may be involved in mechanisms of ethanol-induced endotoxemia. However, it is unclear how ethanol affects absorption of endotoxin from the intestine in vivo. Methods: We gave 10 mg/kg of lipopolysaccharides to rats with water (group 1), 5% ethanol (group 2), or 20% ethanol (group 3) using an intubation tube to the stomach. Blood samples were collected and plasma endotoxin levels were measured. We used fluorescence spectrophotometer to examine permeability of the gut to macromolecules (fluorescein isothiocyanate-dextran; 4,000 Da [FD4] or 20,000 Da [FD20]). Results: Plasma endotoxin levels were not different between group 1 (9 ± 2 pg/ml) and group 2 (14 ± 3 pg/ml), whereas they significantly increased in group 3 with a peak at 60 min (87 ± 35 pg/ml). Acute ethanol administration did not affect clearance of endotoxin in rats. Hemorrhagic erosions of the proximal small intestine with epithelial cell loss were observed in group 3 at 4 hr, but no significant histological change was observed at 30 min by light microscopy. Acute ethanol administration (20%) increased the permeability of the small intestine to FD4 and FD20 in 30 min when no hemorrhagic erosions of the proximal small intestine with epithelial cell loss were observed. Conclusions: Acute ethanol administration increases intestinal permeability before pathological changes are revealed by light microscopy. Acute ethanol ingestion, especially at high concentrations, facilitates the absorption of endotoxin from rats' small intestine via an increase in intestinal permeability, which may play an important role in endotoxemia observed in alcoholic liver injury. [source]

    Plasma levels of tumour necrosis factor- , in patients with chronic periodontitis and type 2 diabetes

    JOURNAL OF CLINICAL PERIODONTOLOGY, Issue 1 2007
    S. Engebretson
    Abstract Objectives: Studies suggest that elevated circulating tumour necrosis factor- , (TNF- ,) may contribute to insulin resistance in patients with type 2 diabetes. The source of plasma TNF has been thought to be adipocytes associated with obesity, but inflammation and infection result in TNF- , production as well. Methods: We studied 46 patients with type 2 diabetes and chronic periodontitis to determine the relationship between plasma TNF- , levels and clinical measures of periodontitis, gingival crevicular fluid (GCF) interleukin-1, (IL-1,), plasma endotoxin, serum glucose, and glycated haemoglobin (HbA1c). TNF- , levels were measured using a high sensitivity enzyme-linked immunosorbent assay. Results: TNF- , showed a significant positive correlation with attachment loss (r=0.40, p=0.009), plasma endotoxin (r=0.33, p=0.03), and GCF IL-1, (r=0.33, p=0.035), but not probing depth (r=0.28, p=0.07), bleeding on probing (r=0.30, p=0.053), plaque index (r=0.22, p=0.17), serum glucose, HbA1c (r=0.10, p=0.50), or body mass index (r=0.077, p=0.62). A dose,response relationship was observed between periodontitis severity and TNF- , (p=0.012). Conclusion: The finding that chronic periodontitis is associated with plasma TNF- , levels in subjects with type 2 diabetes supports the hypothesis that periodontal infection and inflammation may contribute to insulin resistance. [source]

    Effect of Acute Ethanol Administration on the Intestinal Absorption of Endotoxin in Rats

    ALCOHOLISM, Issue 3 2000
    Hironao Tamai
    Background: Endotoxin has been implicated in the pathogenesis and progression of alcoholic liver disease. Not only inactivation of reticuloendothelial function, which reduces clearance of endotoxin, but also an increase in absorption of endotoxin from the intestine may be involved in mechanisms of ethanol-induced endotoxemia. However, it is unclear how ethanol affects absorption of endotoxin from the intestine in vivo. Methods: We gave 10 mg/kg of lipopolysaccharides to rats with water (group 1), 5% ethanol (group 2), or 20% ethanol (group 3) using an intubation tube to the stomach. Blood samples were collected and plasma endotoxin levels were measured. We used fluorescence spectrophotometer to examine permeability of the gut to macromolecules (fluorescein isothiocyanate-dextran; 4,000 Da [FD4] or 20,000 Da [FD20]). Results: Plasma endotoxin levels were not different between group 1 (9 ± 2 pg/ml) and group 2 (14 ± 3 pg/ml), whereas they significantly increased in group 3 with a peak at 60 min (87 ± 35 pg/ml). Acute ethanol administration did not affect clearance of endotoxin in rats. Hemorrhagic erosions of the proximal small intestine with epithelial cell loss were observed in group 3 at 4 hr, but no significant histological change was observed at 30 min by light microscopy. Acute ethanol administration (20%) increased the permeability of the small intestine to FD4 and FD20 in 30 min when no hemorrhagic erosions of the proximal small intestine with epithelial cell loss were observed. Conclusions: Acute ethanol administration increases intestinal permeability before pathological changes are revealed by light microscopy. Acute ethanol ingestion, especially at high concentrations, facilitates the absorption of endotoxin from rats' small intestine via an increase in intestinal permeability, which may play an important role in endotoxemia observed in alcoholic liver injury. [source]

    Intestinal decontamination improves liver haemodynamics in patients with alcohol-related decompensated cirrhosis

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 9 2009
    J. VLACHOGIANNAKOS
    Summary Background, Endotoxaemia is commonly seen in cirrhotic patients with ascites and this may be associated with increased portal pressure. Aim, To investigate the effect of intestinal decontamination on liver haemodynamics in alcohol-related cirrhotic patients with ascites. Methods, We included 30 patients. At day 0, systemic and splanchnic circulation endotoxin levels were determined and HVPG measurement performed. Patients received rifaximin (1200 mg/day) for 28 days. At day 29, systemic and splanchnic circulation endotoxin levels were determined and HVPG measurement performed again. Results, Median (range) plasma endotoxin levels decreased significantly after rifaximin administration both in systemic [1.45(0,3.1) vs. 0.7(0,2.7), P < 0.0001] and splanchnic circulation [1.8(0,3.4) vs. 0.8(0,2.1), P < 0.0001]. Meanwhile, the difference seen in endotoxin levels between the splanchnic and systemic circulation at day 0 (P = 0.001) was not noted at day 29 (P = 0.137). HVPG measurement was possible in 28 patients. Median (range) HVPG values were 18 mmHg (12.7,26.3) on day 0 vs. 14.7 mmHg (7,20) on day 29 (P < 0.0001). HVPG decreased after rifaximin in 23, remained stable in two and increased in three patients. Conclusion, Hepatic venous pressure gradient values decreased significantly after intestinal decontamination with rifaximin in patients with alcohol-related decompensated cirrhosis and this might have been achieved through significant reduction of plasma endotoxin levels. [source]

    Effects of probiotic therapy on portal pressure in patients with cirrhosis: a pilot study

    LIVER INTERNATIONAL, Issue 7 2009
    Puneeta Tandon
    Abstract Background: Recent literature has supported the role of bacterial translocation as a mediator of splanchnic vasodilatation and portal hypertension. The objective of this study was to determine whether the probiotic VSL#3 would reduce portal pressure in patients with cirrhosis. Methods: Eight patients with compensated or very early decompensated cirrhosis and hepatic venous pressure gradient (HVPG) >10 mmHg, received 2 months of VSL#3 (3600 billion bacteria daily). The HVPG, intestinal permeability, endotoxin, tumour necrosis factor (TNF)-,, interleukin (IL)-6, IL-8, renin and aldosterone were measured at baseline and study end. Results: There was no change in the HVPG or intestinal permeability from baseline to study end but there was a trend to reduction in plasma endotoxin (P=0.09), a mild but significant increase in serum TNF-, (P=0.02) and a significant reduction in plasma aldosterone (P=0.03). Conclusions: Within the limitations of small sample size, there does not appear to be a benefit of probiotic therapy for portal pressure reduction in patients with compensated or early decompensated cirrhosis. The reductions in endotoxin and aldosterone suggest possible beneficial effects of probiotics for this patient population. The clinical significance of the small but unexpected increase in TNF-, is unclear. Future studies are planned in patients with decompensated cirrhosis. [source]