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PubMed2004

Effects of propofol on endotoxin-induced acute lung injury in rabbit.

This study was undertaken to clarify the effects of propofol on endotoxin-induced acute lung injury. Rabbits were randomly assigned to one of four groups. Each group received intravenous infusion of saline only, saline and Escherichia coli endotoxin, propofol (1 mg/kg bolus, then 5 mg/kg/hr) and endotoxin, or propofol (4 mg/kg bolus, then 20 mg/kg/hr) and endotoxin respectively. Infusion of saline or propofol was started 0.5 hr before the infusion of saline or endotoxin, and continued for 6 hr thereafter. The lungs of rabbits were ventilated with 40% oxygen. Mean blood pressure, heart rate, arterial oxygen tension (PaO2), and peripheral blood leukocyte and platelet count were recorded. The wet/dry (W/D) weight ratio of lung and lung injury score were measured, and analysis of bronchoalveolar lavage fluid (BALF) was done. Endotoxin decreased PaO2, and peripheral blood leukocyte and platelet count. And it increased W/D ratio of lung, lung injury score and leukocyte count, percentage of PMN cells, concentration of albumin, thromboxane B2 and IL-8 in BALF. Propofol attenuated all these changes except the leukocyte count in peripheral blood. In conclusion, propofol attenuated endotoxin-induced acute lung injury in rabbits mainly by inhibiting neutrophil and IL-8 responses, which may play a central role in sepsis-related lung injury.

Acute Disease↗
PubMed1981

Rectal temperature and blood chemical responses of young chickens given E. coli endotoxin.

Two experiments were conducted to investigate the effect of intravenous injections of bacterial endotoxin in broiler chicks. In both experiments 5-weeks-old chicks were given a single intravenous injection of either distilled water (control) or 1 mg/kg Escherichia coli endotoxin (serotype 0.127:B8) in a volume of 1 mg/kg. In Experiment 1 rectal body temperatures were taken every hour for 24 hr postinjection. In Experiment 2, rectal temperatures and blood samples were taken at 3, 6, 9, 12, 15, and 24 hr following the administration of endotoxin. Hematocrits and plasma glucose, protein, sodium, potassium, magnesium, calcium, and inorganic phosphorus were measured at each time interval. Birds receiving endotoxin showed a significant increase in rectal temperature from 2 hr until 17 hr postinjection. The febrile response was biphasic with temperatures peaking at 3 to 5 hr and again at 9 to 12 hr. No significant changes in hematocrits occurred following endotoxin injection. Plasma protein, potassium, and calcium decreased significantly, while glucose increased significantly after endotoxin administration. No significant changes in plasma magnesium, sodium, or inorganic phosphorus were observed in endotoxin-treated chicks.

Animals↗
PubMed2003

Endotoxins of enteric pathogens modulate the functions of human neutrophils and lymphocytes.

The locomotor responses of human peripheral blood neutrophils and lymphocytes were measured by the change from spherical to polarized shapes in the presence of endotoxins (lipopolysaccharide, LPS) of enteric pathogens: S. dysenteriae type 1, V. cholerae Inaba 569B, S. typhimurium, and K. pneumoniae. We reported earlier that these endotoxins are chemotactic factors for the neutrophils since they stimulated cell polarization within a few minutes of incubation. Endotoxins had an inhibitory effect upon neutrophil phagocytosis of opsonized yeast and the cells engulfed fewer yeasts. Interestingly, endotoxins increased neutrophil adhesion to clean glass surfaces, but stimulated the cells to exhibit increased random locomotion (chemokinesis) through cellulose nitrate filters and show an enhanced ability to reduce nitroblue tetrazolium (NBT) dye. Unlike neutrophils, lymphocytes direct from blood do not show polarized morphology towards chemotactic factors but the cells acquire locomotor capacity during 24-72 h culture with mitogens such as phytohemagglutinin (PHA), phorbol myristate acetate or concanavalin A. Stimulation of blood lymphocytes with endotoxins did not induce cell polarization in short-term but long-term culture resulted in an increase in the proportion of polarized cells that acquired locomotor morphologies. The majority of these cells were identified as esterase negative B-lymphocytes that migrated through filters. Despite the optimum time of incubation for each of these cell types being different, we found that lymphocytes respond to much lower concentrations of endotoxins than the neutrophils. These findings suggest that endotoxins of enteric pathogens modulate the functions of human blood neutrophils and lymphocytes.

Adult↗
PubMed1998

[Level of bacterial endotoxins in Haemophilus influenzae type b vaccines conjugated with toxoids (td, Di)].

Quantitative evaluation of bacterial endotoxin was performed in the following vaccines: Act-Hib, Hiberix, Hib-Titer. The aim of this study was to assess the accuracy and precision of chromogenic LAL test with S-2423 substrate for this particular biopreparations and after that to determine the amounts of endotoxin as a factor of vaccine safety. Because of the lack of information concerning the presence of endotoxin in Act-Hib vaccine, we also tried to establish the limits for the presence of endotoxin in this type of vaccine. The estimated level of endotoxin was as follows: 110 EU/ml in Act-Hib, 1.64 EU/ml in Hiberix and 2.4 EU/ml in Hib-Titer. The results of this study showed that the amounts of endotoxin was dependent on the molecular size of polysaccharide PRP and on the presence of protein component. The limit of endotoxin presence in Act-Hib vaccine recommended by us is max. 150 EU/ml.

Endotoxins↗
PubMed1999

Effects of inhalation of dust and endotoxin on respiratory tracts of pigs.

OBJECTIVE: To assess the effects of inhalation of feed flour dust and dustborne endotoxin on respiratory tracts of pigs. ANIMALS: 29 healthy Belgian Landrace pigs. PROCEDURE: Pigs housed in an environmental chamber were exposed for 6 days to feed flour dust (1 to 15 mg/m3) and dustborne endotoxins (50 to 2,500 ng/m3). Effects were evaluated by measuring albumin concentration, lactate dehydrogenase (LDH) activity, cell composition of nasal lavage (NL) and bronchoalveolar lavage (BAL) fluids and blood, and percentages of CD4+ and CD8+ T lymphocytes in blood and lavage fluids. Dustborne endotoxin was obtained by mixing endotoxins from Escherichia coli (serotype O127:B8) with feed flour before spraying the flour in the environmental chamber. RESULTS: Exposure did not affect cell composition of NL fluid or blood. Total cell counts of BAL fluids were increased in all groups exposed to dust. Macrophage counts were increased in pigs exposed to inhalable dust concentrations as low as 4.4 mg/m3, and lymphocyte counts were increased in groups exposed to high dust concentrations. Percentages of CD4+ and CD8+ T lymphocytes in blood and lavage fluids were unchanged. In all dust-exposed groups, albumin content of BAL fluid was increased, whereas LDH activity was unaffected. Macrophage and lymphocyte infiltration and edema in the bronchi were identified by light microscopy. Effects attributable to E. coli endotoxin exposure were not identified. CONCLUSIONS: Inhalation of feed flour dust did not affect nasal mucosa but did induce bronchial airway inflammation. Dustborne endotoxins did not have effects attributable to endotoxin alone.

Albumins↗
PubMed1999

Endotoxin-endothelium interactions in "low-perfusion state" research.

LPS/endotoxin provokes a plethora of pathological events some of which may be considered as examples of "low perfusion state". These are discussed here. It is well known that hypotension and refractoriness to vasocostrictors are the hallmark of endotoxic shock. Nevertheless, there are some vascular beds, such as mesenteric circulation, that respond with vasoconstriction - not vasodilation to endotoxin. Aminoguanidine, an inhibitor of NOS-2, blocks endotoxin- induced increase of resistance in mesenteric bed and endotoxin-induced translocation of bacteria through the gut wall. It is postulatede that endotoxin has antiarrythmogenic action due to the release of nitric oxide and increase in intracellular cGMP levels. Although we demonstrate that endotoxin increases nitric oxide formation in spleen and liver, its contribution to the injury of these organs by endotoxin is not fully established. In addition, we present our immunochemistry data on nitrotyrosine formation in the liver and spleen of endotoxin-treated animals.

Anesthesia↗
PubMed2000

Endotoxin-triggered haematological interactions in Fusobacterium necrophorum infections.

The haematological mechanisms in the course of liver abscess formation were evaluated. They were examined by employing viable cells of Fusobacterium necrophorum subsp. necrophorum and Fusobacterium necrophorum subsp. funduliforme in comparison with their endotoxins. Whole cell infection with F.n. necrophorum led to neutrophilia and to a concomitant monocytosis in parallel with those responses induced by the in vivo injection of its endotoxin. Viable infection with F.n. funduliforme was characterized by a sustained endotoxin-related monocytosis against neutropenia. The stimulatory impact of endotoxin on monocytes when released from a viable F.n. funduliforme infection suggested an inherently peculiar mechanism which differed from the induction of both neutrophilia and monocytosis when F.n. funduliforme endotoxin was administered alone. The neutrophilic inducing capacity of the F.n. necrophorum endotoxin was equally illustrated by its positive chemotactic effect on polymorphonuclear neutrophils in vitro. The data presented here emphasize the virulence of F.n. necrophorum viewed in reference to changes in leucocyte trafficking and as complemented by a relatively high endotoxin content.

Animals↗
PubMed2000

Inhibition of endotoxin effects on cultured human middle ear epithelium by bactericidal permeability-increasing protein.

HYPOTHESIS/BACKGROUND: Endotoxin can induce morphologic changes to middle ear epithelium, which can disturb the mucociliary clearance system (MCS) and lead to otitis media with effusion (OME). The bactericidal/permeability-increasing (BPI) protein is a major component of neutrophil granules and binds with high affinity to endotoxin. In this study, the capacity to inhibit the effects of endotoxin by rBPI21, a recombinant amino-terminal analog derived from BPI, was investigated on cultured human middle ear epithelium using light microscopy and scanning- and transmission electron microscopy. METHODS: Human middle ear epithelium was air-exposed cultured on a collagenous underlayer with different additions of endotoxin and rBPI21 to the culture medium. The tissue specimens were inspected after 4 weeks for the number of ciliated and secretory cells, thickness of the mucosal layer, and cell size. RESULTS: The morphologic changes induced by endotoxin were increased thickness of the mucosal layer and increased number of secretory cells. These changes were significantly diminished or even absent when endotoxin was added with rBPI21 to the culture medium. CONCLUSION: rBPI21 can inhibit morphologic changes in the middle ear epithelium due to endotoxin. Hence, the authors believe that rBPI21 can be a new therapeutic agent in the treatment of OME.

Anti-Bacterial Agents↗
PubMed2001

[Effect of tobramycin with topical diclofenac on arachidonic acid in endotoxin-induced uveitis].

PURPOSE: We studied if tobramycin associated to sodium diclofenac modifies the drug effect of the latter on arachidonic acid metabolism in an endotoxin induced uveitis (EIU) model in albino rabbits. METHODS: Experimental uveitis was induced by intravitreal injection of a 10 ng lipopolysaccharide A Salmonella typhimurium endotoxin dissolved in 5 microl saline solution in the right eye of experimental animals. We have used 48 animals (4 groups of 12 animals each). The control group (G-I) was injected with saline solution (5 microl); the endotoxin group (G-II) was injected with 5 microl of ET; group III and IV were injected with the same amount of ET and treated with topical sodium diclofenac (1%) (Group III) and tobramycin and sodium diclofenac (0.3%) (Group IV) two hours before the administration of endotoxin and then every two hours until 24 hours, when we determined E2 prostaglandin and B4 leukotriene concentration in aqueous humor obtained by paracentesis of the anterior chamber. RESULTS: We observed how the E2 prostaglandin concentration was reduced in the two treatment groups compared with the endotoxin group (p<0.01). However, there were no differences between groups III and IV (p>0.01). There was a mild increase of B4 leukotriene in both treatment groups, which was not significant in relationship to the endotoxin group (p>0.01). No differences were found between the two treatment groups (p>0.01). CONCLUSION: Using the association of tobramycin does not affect the action of sodium diclofenac in arachidonic acid metabolism in endotoxin induced uveitis.

Animals↗
PubMed1998

[In vitro analysis of cross immunoreaction between CGRP and endotoxin in CGRP radioimmunoassay].

In the present study, the effect of endotoxin on the radioimmunoassay of calcitonin gene-related peptide (CGRP) was investigated by method of radioimmunoassay. The results showed a competitive combination of endotoxin at high-concentrations (higher than 5 micrograms/ml) with multiclonal antibody of CGRP, and the cross immunoreaction ratio between CGRP and endotoxin was 5.6 x 10(-6). The mixed endotoxin in samples was effectively cleared through C18 column purification. The data indicated that endotoxin interfered CGRP radioimmunoassay in vitro at high concentrations. The influence of endotoxin on CGRP radioimmunoassay can be avoided through C18 column purification for the endotoxin-containing samples.

Animals↗
PubMed2001

Exposure assessment to airborne endotoxin, dust, ammonia, hydrogen sulfide and carbon dioxide in open style swine houses.

Information is limited for the exposure levels of airborne hazardous substances in swine feed buildings that are not completely enclosed. Open-style breeding, growing and finishing swine houses in six farms in subtropical Taiwan were studied for the airborne concentrations of endotoxin, dust, ammonia, hydrogen sulfide and carbon dioxide. The air in the farrowing and nursery stalls as partially enclosed was also simultaneously evaluated. Three selected gases and airborne dusts were quantified respectively by using Drager diffusion tubes and a filter-weighing method. Endotoxin was analyzed by the Limulus amoebocyte lysate assay. Average concentration of airborne total endotoxin among piggeries was between 36.8 and 298 EU/m(3), while that for respirable endotoxin was 14.1-129 EU/m(3). Mean concentration of total dust was between 0.15 and 0.34 mg/m(3), with average level of respirable dust of 0.14 mg/m(3). The respective concentrations of NH3, CO2 and H2S were less than 5 ppm, 600-895 ppm and less than 0.2 ppm. Airborne concentrations of total dust and endotoxin in the nursery house were higher than in the other types of swine houses. The finishing house presented the highest exposure risk to NH3, CO2 and H2S. Employees working in the finishing stalls were also exposed to the highest airborne levels of respirable endotoxin and dust. On the other hand, the air of the breeding units was the least contaminated in terms of airborne endotoxin, dust, NH3, CO2 and H2S. The airborne concentrations of substances measured in the present study were all lower than most of published studies conducted in mainly enclosed swine buildings. Distinct characteristics, including maintaining swine houses in an open status and frequent spraying water inside the stalls, significantly reduce accumulation of gases and airborne particulates.

Air Pollution, Indoor↗
PubMed2001

Hepatic encephalopathy in rats with thioacetamide-induced fulminant hepatic failure: role of endotoxin and tumor necrosis factor-alpha.

BACKGROUND: Hepatic encephalopathy, a complex neuropsychiatric syndrome secondary to acute liver failure, chronic parenchymal liver disease or portal-systemic shunting, may possibly develop through mediators of endotoxin and tumor necrosis factor-alpha (TNF-alpha). However, there are no published data concerning the relationships between the severity of encephalopathy and the plasma levels of endotoxin and TNF-alpha. METHODS: Male Sprague-Dawley rats weighing about 300-350 g were used. Fulminant hepatic failure was induced by intraperitoneal injection ofthioacetamide (350 mg/kg/day) for 3 consecutive days. Severity of encephalopathy was assessed by measuring motor counts using an Opto-Varimex animal activity meter. Plasma levels of endotoxin and TNF-alpha were determined by chromogenic Limulus assay and ELISA method, respectively. RESULTS: Our study revealed that higher plasma levels of endotoxin (> 5.9 pg/ml) and TNF-alpha (> 18.8 pg/ml) were significantly associated with more blunted motor activities in rats with fulminant hepatic failure (p < 0.05). A significant correlation was observed between plasma concentrations of endotoxin and TNF-alpha (r = 0.59, p < 0.001). Plasma levels of endotoxin were weakly correlated with the total movements in an open field (r = -0.34, p = 0.032) and the counts of ambulatory (r = -0.38, p = 0.014) and vertical movements (r = -0.40, p = 0.010). There were no correlations between the motor counts and plasma levels of TNF-alpha (p > 0.05). CONCLUSIONS: In addition to endotoxin and TNF-alpha, other factors may participate in the pathogenesis of hepatic encephalopathy in rats with thioacetamide-induced fulminant hepatic failure.

Animals↗
PubMed2001

A model for predicting endotoxin concentrations in metalworking fluid sumps in small machine shops.

METHODS: In British Columbia, Canada, nineteen small machine shops which used water-based metalworking fluids (MWF) were examined. One bulk MWF sample was taken from each independent sump (N=140) and tested for endotoxin using the Limulus Amoebocyte Lysate assay. Factors that might influence the MWF sump endotoxin concentration were investigated using mixed effect multiple regression modelling to control for repeated measures within shops. RESULTS: The geometric mean (GM) endotoxin concentration was 6791 EU/ml. Contamination of MWF with tramp oil, MWF pH, MWF temperature, and MWF type were significant predictors of sump fluid endotoxin concentration (model P=0.0001, ordinary least squares R(2) =0.36). Concentrations of endotoxin in sump fluids were increased by MWF contamination with tramp oils such as hydraulic oils, preservative oils, spindle oils, slidway lubricants, gear lubricants, and greases (model predicted GM=17400 EU/ml vs. 1600 EU/ml without tramp oil). Concentrations were also elevated where pH was lower than 8.5 (predicted GM=10600, vs 3600 EU/ml for pH 8.5 to 9.5), where soluble fluids were used (predicted GM=11800 vs. 2800 EU/ml for synthetic fluids), and where sump fluid temperatures were higher (predicted GM=2600 EU/ml at 11 degrees C vs. 21500 EU/ml at 32 degrees C). The within-shop correlation of sump bulk fluid endotoxin concentrations was 38%. CONCLUSIONS: Minimizing tramp oil contamination, using synthetic fluids, and monitoring pH and temperature would be valuable tools for controlling endotoxin contamination in MWF sumps. In addition, since there was correlation within-shop, contamination of one sump in a shop may suggest changing the fluids in all.

Endotoxins↗
PubMed2001

The role of immune activation in endotoxin-induced atherogenesis.

Some infectious agents may contribute to atherosclerosis by maintaining a heightened state of inflammatory response. Although the risk for atherosclerosis was associated with elevated plasma levels of endotoxin, it is difficult to firmly establish what place endotoxin assumes in the etiology of this disease. As the ability for endotoxin to promote disease may depend on its ability to initiate an inflammatory response, it may be controlled by additional regulatory factors. We measured plasma levels of endotoxin and serum levels of neopterin and soluble interleukin-2 receptor in a random population of 402 men and women, 50-79 years old at the 1990 baseline evaluation (Bruneck Study). End point of the prospective survey was incident (early) atherosclerosis in the carotid arteries as assessed with duplex ultrasound. Subjects with high endotoxin levels (90th percentile) in combination with low neopterin or soluble interleukin-2 receptor levels (below median) did not differ from those with low endotoxin in their risk of incident atherosclerosis. The risk associated with high endotoxin, however, was markedly elevated in subjects with high (above median) neopterin or soluble interleukin-2 receptor levels. The study provides epidemiological evidence that the atherogenic potential of endotoxemia is affected by concomitant immune activation.

Aged↗
PubMed2002

Endotoxin tolerance: a review.

Endotoxin tolerance was initially described when it was observed that animals survived a lethal dose of bacterial endotoxin if they had been previously treated with a sublethal injection. In animal models, two phases of endotoxin tolerance are described, an early phase associated with altered cellular activation and a late phase associated with the development of specific antibodies against the polysaccharide side chain of Gram-negative organisms. Recently, there has been a tremendous resurgence of interest in the mechanisms responsible for altered responsiveness to bacterial endotoxin. Host immune cells, particularly macrophages and monocytes, that are exposed to endotoxin for 3 to 24 hrs are rendered "tolerant" and manifest a profoundly altered response when rechallenged with bacterial endotoxin or lipopolysaccharide. The "lipopolysaccharide-tolerant" phenotype is characterized by inhibition of lipopolysaccharide-stimulated tumor necrosis factor production, altered interleukin-1 and interleukin-6 release, enhanced cyclooxygenase-2 activation, inhibition of mitogen-activated protein kinase activation, and impaired nuclear factor-kappa B translocation. Human monocytes and macrophages can be induced to become tolerant, and there is increasing evidence that monocytic cells from patients with systemic inflammatory response syndrome and sepsis have many characteristics of endotoxin tolerance.

Animals↗
PubMed1992

In vivo and in vitro effects of endotoxin on vascular responsiveness to norepinephrine and signal transduction in the rat.

We investigated, after in vitro and in vivo exposure to gram-negative endotoxin, the altered responsiveness of rat aortic smooth muscle to catecholamines. Two hour exposure of aortic rings from normal rats to 100 ng/ml of Escherichia coli 0111:B4 endotoxin in vitro in an artificial medium supplemented with 5% fetal calf serum at 37 degrees C did not effect the basal and norepinephrine (NE)-stimulated (10 microM, 1 hr, 37 degrees C) phosphoinositide (PI) hydrolysis and isometric contractions induced by graded doses (1 nM to 10.0 microM) of NE. Increasing the incubation time with endotoxin to 18 hr did not alter the basal PI hydrolysis but significantly (P less than 0.05) decreased the NE-induced PI hydrolysis (30% inhibition) and contractile sensitivity to NE (increase of EC50 from 20.0 +/- 3.8 to 156.4 +/- 46.7 nM). Qualitatively similar results were obtained in experiments where rats were injected intravenously with buffer or an LD50 dose (10 mg/kg) of endotoxin. In these ex vivo measurements, only an 18 hr exposure to endotoxin caused significant (P less than 0.001) decreases in basal (58% inhibition) and NE-stimulated (75% inhibition) PI hydrolysis and in NE-induced isometric contractions (increase of EC50 from 11.0 +/- 3.3 to 664.1 +/- 280.0 nM). The results show that the endotoxin-induced hyporeactivity to alpha 1-adrenergic receptor stimulation 1) is markedly dependent on the length of endotoxin exposure, 2) does not require (although may be enhanced by) contact with blood cells and plasma, and 3) is paralleled by a decrease in both basal and NE-stimulated PI hydrolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Endotoxin-induced production of interleukin 6 by equine peritoneal macrophages in vitro.

A study was performed to determine whether equine peritoneal macrophages produce interleukin 6 (IL-6) in vitro in response to endotoxin. Peritoneal fluid was collected from 14 clinically normal adult horses and was used as the source of peritoneal macrophages. Macrophages from each horse were isolated and cultured separately in vitro in the absence or presence of various concentrations (0.5, 5, 500 ng/ml) of endotoxin (lipopolysaccharide from Escherichia coli 055:B5). Culture medium supernatants were collected after 3, 6, 12, and 24 hours' incubation and were frozen at -70 C until assayed for IL-6 activity. Supernatant IL-6 activity was determined by use of a modified colorimetric assay and the murine hybridoma cell line B 13.29 clone B.9, which is dependent on IL-6 for survival. Results indicated that equine peritoneal macrophages produce IL-6 in vitro and that supernatant medium IL-6 activity was significantly (P less than 0.05) increased by exposure to endotoxin. Significant (P less than 0.05) time and treatment effects on macrophage IL-6 production were apparent. The IL-6 activity peaked at 6 or 12 hours' incubation, then remained high through 24 hours' incubation, regardless of endotoxin exposure. Medium IL-6 activity during 3 and 6 hours' incubation was significantly (P less than 0.05) greater in macrophages exposed to 5 or 500 ng of endotoxin/ml than in those exposed to 0.5 ng of endotoxin/ml; however peak IL-6 activity was similar among all endotoxin concentrations. Endotoxin concentration did not have an effect on medium IL-6 activity from macrophages exposed to endotoxin for 12 or 24 hours.

Animals↗
PubMed2004

Effect of ketamine on NF-kappa B activity and TNF-alpha production in endotoxin-treated rats.

The effects of ketamine on endotoxin-induced NF-kappaB activation and TNF-alpha expression were studied in vivo. A sepsis model was created by bolus injection of endotoxin (5 mg/kg) into the tail vein of adult Wistar rats. The rats were immediately treated with various doses of ketamine (0.5, 5, or 50 mg/kg) or 0.9% NaCl (10 ml/kg) i.p. At 1, 4, or 6 hr post-treatment, NF-kappaB and TNF-alpha were assayed in the intestine, liver, and lung by electrophoretic mobility shift assay (EMSA) and reverse-transcription polymerase chain reaction (RT-PCR), respectively. Serum TNF-alpha was analyzed by ELISA. Endotoxin enhanced NF-kappaB activity and TNF-alpha expression in the intestine, liver, and lung and it increased TNF-alpha concentration in serum. Ketamine dosages 0.5 mg/kg suppressed the endotoxin-induced NF-kappaB activation and TNF-alpha expression in the intestine. The lowest dose to inhibit NF-kappaB activity and TNF-alpha expression in the lung was 5 mg/kg. Ketamine did not inhibit endotoxin-induced NF-kappaB activity or TNF-alpha expression in the liver; ketamine itself at a dose of 50 mg/kg enhanced NF-kappaB activity and TNF-alpha expression in the liver. Ketamine dosage 0.5 mg/kg inhibited endotoxin-induced TNF-alpha elevation in the serum. In conclusion, ketamine can suppress the induction of NF-kappaB and TNF-alpha by endotoxin in vivo. Subanesthetic dosages of ketamine have an anti-inflammatory effect, but large dosages may be harmful.

Animals↗