Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ENDOTOXINS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,675 records · Page 93Linked to original sources
PubMed1986

The effect of endotoxin and prostaglandin E2 on the proliferation of keratinocytes in vitro.

Since the rate of epidermal basal cell proliferation appears to be a crucial factor in the development of acquired cholesteatoma, we studied the effect of prostaglandin E2 (PGE2) and endotoxin on the growth of keratinocytes. PGE2 and endotoxins are inflammatory mediators in chronic otitis media. Various concentrations of endotoxin and PGE2 were added to keratinocytes derived from newborn rats. The synthesis of DNA was then studied by incorporation of 3H-thymidine into the keratinocytes. We found that either endotoxin or PGE2 alone inhibited DNA synthesis by keratinocytes, while endotoxin (10 micrograms/ml) and PGE2 (10 ng/ml) together stimulated DNA synthesis by keratinocytes. These findings suggest that inflammatory mediators, such as endotoxin plus PGE2, in chronic otitis media stimulate the growth of epidermal basal cells of cholesteatoma.

Animals↗
PubMed1990

Ocular inflammatory effects of intravitreally injected tumor necrosis factor-alpha and endotoxin.

Intravitreal injection of human recombinant tumor necrosis factor-alpha (TNF) induced inflammation in the rabbit eye characterized by dilation of blood vessels in the iris, disruption of the blood-ocular barriers, infiltration of inflammatory cells into the anterior chamber, and accumulation of prostaglandin E in intraocular fluids. Inflammation first appeared on day 1, increased on day 2, and remained elevated on day 7. The inflammatory cell infiltrate in the anterior segment of the eye was largely monocytic on days 1 and 2; by day 7 large numbers of lymphocytes were also present. TNF-induced ocular inflammation therefore differed from that reported for intravitreally injected endotoxin in terms of time course and the types of inflammatory cells in the aqueous humor. In a series of experiments in which combinations of TNF and endotoxin were used, intravitreal injection of TNF, 24 h after a low dose of Escherichia coli endotoxin, produced no more inflammation than that produced by TNF following an injection of endotoxin vehicle. However, if TNF was injected 24 h before endotoxin, the resulting inflammation was greater than that observed in animals given TNF followed by endotoxin vehicle.

Animals↗
PubMed1990

Preimplantation murine embryos are more resistant than human embryos to bacterial endotoxins.

Bacterial endotoxins have been correlated with increased fragmentation of early cleavage-stage human embryos and decreased pregnancy rates in human in vitro fertilization programs. The purpose of the present study was to test the direct effects of increasing concentrations of endotoxins on in vitro fertilization and development of mouse embryos to the blastocyst stage. Sexually mature B6D2F1 female mice were superovulated and oocytecumulus complexes were collected from the oviducts and randomized into control and treatment groups. Oocytes (n = 867) were inseminated with capacitated sperm. Treatments included Ham's F-10 supplemented with 3 mg/ml bovine serum albumin and increasing amounts of endotoxin (0.35, 0.64, 0.92, 1.5, 2.08, 3.21, 6.07, and 11.79 ng/ml). Percentage cleavage, percentage fragmentation at the four-cell stage, and percentage expanded blastocyst formation (of cleaved embryos) were evaluated. Statistically significant decreases in cleavage at 6.07 ng/ml (P less than 0.05) and blastocyst formation at 11.79 ng/ml (P less than 0.05) of endotoxin were observed. Fragmentation at the four-cell stage was significantly increased at 3.21 ng/ml (P less than 0.05) of endotoxin. We conclude that the levels of endotoxin necessary to decrease murine preimplantation development significantly is higher than that reported for human embryos.

Animals↗
PubMed1982

Effect of colistin on reduction of biliary flow induced by endotoxin in E. coli.

In order to evaluate whether an antiendotoxin agent can inhibit the action of endotoxin of Escherichia coli on biliary flow, we used 18 models of isolated perfused pig liver divided into four groups: (A) five perfused livers (control), (B) five perfused livers with 2 mg/100 ml of endotoxin added, (C) five perfused livers with 2 mg/100 ml of endotoxin added and treated with 1,500,000 IU of colistin, and (D) three perfused livers with 1,500,000 IU of colistin with no endotoxin. The livers were isolated and perfused according to a technique previously described by our laboratory. The viability of the perfusions was controlled by means of the mitochondrial respiration test. Transaminase and LDH levels were measured in the perfused circuit. A significant reduction of the biliary flow was found in the group with endotoxin of Escherichia coli (P less than 0.002). There was no reduction of biliary flow after addition of 1,500,000 IU of colistin (P less than 0.001). No significant changes were observed in the other parameters measured, and no increase of the bile flow was observed in the colistin group. From our results we conclude that colistin is an inhibitor in vitro of the diminished biliary flow induced by endotoxin of Escherichia coli.

Alkaline Phosphatase↗
PubMedDate not supplied

Comparison of the binding of gram-negative bacterial endotoxin by polymyxin B sulphate, colistin sulphate and colistin sulphomethate sodium.

Polymyxins are cyclic polypeptide antibiotics. In addition to their bactericidal activity they bind lipid A and neutralize the biological effects of bacterial endotoxin. We have studied the three available polymyxin preparations: polymyxin B sulphate (PB), colistin sulphate (CS) and colistin sulphomethate sodium (CMS), and compared their endotoxin binding capacity at equivalent therapeutic dosage. Each polymyxin was bound to a column of Sepharose 4B and challenged with 5 micrograms of endotoxin from Escherichia coli O127:B8. Recovery of endotoxin in the eluate was measured by a quantitative Limulus lysate microassay. PB and CS bound 94% of the challenge dose, CMS 89% and the control column (Sepharose alone) 24%. These results suggest that parenteral CMS (the least toxic polymyxin) retains useful anti-endotoxin capacity, and that in neutropenic patients, oral polymyxin may exert both anti-endotoxin and antimicrobial effects.

Colistin↗
PubMed1979

[Disseminated intravascular coagulation (DIC) after endotoxin infusion into the common bile duct of rabbits (author's transl)].

Endotoxin from E. coli was infused into the distally ligated common bile duct of rabbits under the static pressure of 25 cm H2O. Fibrinogen, soluble fibrin monomer complexes, antithrombin III, leukocyte and platelet counts were estimated before, and 2, 4, and 6 h after endotoxin infusion. All parameters were found significantly changed 2 h after endotoxin infusion. While fibrinogen level, AT III, leukocyte and platelet counts decreased after the endotoxin infusion the amount of SFMC increased. The change of hematological parameters showed a pattern characteristic of disseminated intravascular coagulation (DIC). In accordance with this microclots in the glomeruli of the kidneys could be demonstrated in all endotoxin-treated animals by pathological study. The findings suggest that by endotoxin infusion into the common bile duct, as a focal origin, DIC can be produced.

Animals↗
PubMed1981

Role of leucocyte procoagulant activity in endotoxin-induced DIC: evidence from comparative studies in rats and rabbits.

We have investigated the ability of rat and rabbit leucocytes to generate coagulant activity (PCA) in response to endotoxin in vitro and in vivo. On prolonged incubation with endotoxin (10 microgram/ml f.c.) isolated rabbit leukocytes developed strong PCA as measured by clotting and amidolytic assay. In contrast, rat leucocyte failed to produce any PCA even in the presence of huge amounts of endotoxin (200 microgram/ml f.c.) When rabbits were given two spaced endotoxin injections (25 microgram/kg b.w., 24 h apart) blood leucocytes harvested 30--60 min after the second injection consistently showed marked PCA. Again, unlike injections (up 2 mg/kg b.w.) were completely devoid of PCA. These findings support the view that leucocytes are involved in endotoxin-induced disseminated intravascular coagulation in rabbits. On the other hand the poor response of rat leucocytes to endotoxin might help explain the resistance of rats to DIC and Sanarelli-Shwartzman reaction.

Animals↗
PubMed1992

Endotoxin tolerance and polymyxin B modify liver damage and cholestasis induced by a single dose of alpha-naphthylisothiocyanate in the rat.

A single oral dose of alpha-naphthylisothiocyanate (ANIT) induces intrahepatic cholestasis and endotoxemia in the rat. To assess if a pathogenic relationship between endotoxin and ANIT-induced liver injury could be postulated, rats were pretreated by either induction of endotoxin tolerance, or with the anti-endotoxin agent polymyxin B. A single oral dose (10 or 20 mg/100 g body wt) of ANIT was then given to ascertain whether these methods of modifying endotoxicity would protect the animals against ANIT damage. Both pretreatments significantly reduced the incidence of endotoxemia after ANIT administration, as detected by either lead acetate enhancement method or the Limulus gelation test (LGT). The lethality of a single 20 mg/100 g body wt dose of ANIT was reduced from 55% to 15% by polymyxin B administration, and to 10% by an endotoxin-tolerant state. Moreover, when 10 mg/100 g body wt ANIT was given none of the animals died in 10 days, and the serum levels of bilirubin, alkaline phosphatase (AlPh), gamma-glutamyl transferase (gamma-GT), and transaminases (evaluated 1, 2, and 5 days after treatments) were significantly lower in the endotoxin-tolerant or polymyxin B administered rats; this biochemical protection was mirrored in the lack of histological alteration. The results demonstrate that the modification of endotoxicity offers significant protection against acute liver damage induced by ANIT. Thus the development of endotoxemia may play a pathogenic role in ANIT-induced liver injury. This conclusion is supportive of the hypothesis that endotoxins are necessary for the hepatotoxic agent to exert its full effects.

1-Naphthylisothiocyanate↗
PubMed1986

Plasma endotoxin levels and functions of peripheral granulocytes in surgical patients with respiratory distress syndrome.

Plasma endotoxin levels and granulocyte functions (chemiluminescence and chemotaxis) were determined in fifty-two patients with postoperative sepsis. Seventeen had concurrent respiratory distress syndrome (RDS group) and the remaining thirty-five were free of the syndrome (non-RDS group). The plasma endotoxin concentrations were higher in the RDS group than in the non-RDS group (p less than 0.001). All nine patients with particularly high levels (greater than 80 pg) belonged to the RDS group. We noted a positive correlation in chemiluminescence (p less than 0.001, r = 0.67) and a negative correlation in chemotactic activity (p less than 0.001, r = 0.69). To determine whether endotoxin alters normal granulocyte functions in vitro, healthy granulocytes were treated by the endotoxin (E. coli 0111:B4). There was an increase in chemiluminescence and a decrease in chemotactic activity, as observed in vivo. Furthermore, normal granulocytes chemiluminescence was increased by pretreatment of RDS plasma showing high endotoxin levels in vitro (n = 4, p less than 0.05). Thus, endotoxin in the plasma probably plays an important role in marked changes in peripheral granulocyte functions in patients with respiratory distress syndrome.

Adult↗
PubMed1988

Enhanced survival to endotoxin in guinea pigs fed IV fish oil emulsion.

Improved survival to endotoxin has been demonstrated in rats pretreated with cyclooxygenase inhibitors or made essential fatty acid deficient, implying that excessive omega 6 fatty acids, possibly through their eicosanoid products, contribute to mortality. Following endotoxin administration, we also have shown improvement in survival with oral diets supplemented with fish oil. This study sought to explore whether parenteral fish oil ameliorates the adverse impact of endotoxin. Male Hartley-strain guinea pigs were obtained at a body weight of 500 g and fed a normal laboratory diet. Central venous lines through which the animals received either a 10% safflower oil emulsion (n = 11) or a 10% fish oil emulsion (n = 11) during two, 24-hr periods separated by two days were inserted. Two days after the second infusion, endotoxin (0.35 mg/100 g b.w.), was given intraperitoneally, and survival was noted. The animals received a total of 25.4 g of IV fat per kg b.w., including 5.3 g of eicosapentaenoic acid per kg b.w., for the fish oil group. From six hr after endotoxin through four days, there was better survival in the fish oil group (p less than .006). Final mortality showed 7/11 fish-fed vs 2/11 safflower-fed animals surviving. We conclude that the administration of parenteral fish oil, even for a brief time, can have a profound effect on subsequent survival to endotoxin.

Animals↗
PubMed1992

Endotoxin levels in cirrhotic rats with sterile and infected ascites.

Endotoxin levels were measured in sterile and bacterially infected ascites in a rat model of phenobarbital and carbon tetrachloride induced cirrhosis was used. An improved chromogenic substrate assay was used to measure endotoxin. All rat ascites specimens were positive for endotoxin. In culture-negative ascites (n = 8), it ranged from 0.05 EU/ml to 0.14 EU/ml (0.08 +/- 0.04 EU/ml, mean +/- SD) (Escherichia coli 0111:B4 endotoxin was used as a reference). In culture-positive ascites (premortem n = 3, postmortem n = 1), it ranged from 0.78 EU/ml to 1.8 EU/ml (1.29 +/- 0.59 EU/ml, mean +/- SD). All rats with premortem culture-positive ascites died within two days. This model is useful to study ascites endotoxin levels. In this study, increasing levels of ascites endotoxin correlated with spontaneous bacterial peritonitis and death.

Animals↗
PubMed1987

Quantitative histology of muramyl dipeptide-potentiated induction of tumor necrosis by endotoxins.

Combinations of muramyl dipeptide (MDP) and toxic or detoxified endotoxin induced necrosis and subsequent disappearance of solid Meth A tumors in syngeneic mice. Toxic endotoxin alone was far less effective. MDP and detoxified endotoxin had negligible antitumor effects of their own. These observations were confirmed by histological examination. Neither MDP nor detoxified endotoxin induced significant changes in and around the tumor by 4, 24, and 48 h after intravenous administration when compared with saline treatment. MDP amplified various effects of toxic endotoxin such as the induction of hyperemia, mitotic arrest, mast cell depletion, non-hemorrhagic necrosis and reduction in lymphocyte infiltrates, but did not affect hemorrhagic necrosis or the influx of polymorphonuclear leukocytes. The combination of MDP and detoxified endotoxin lacked the latter two effects, but the other effects were similar to, although slightly less marked than those induced by the toxic combination. Because the degree of hyperemia was proportional to the degree of subsequent non-hemorrhagic necrosis, MDP seems to potentiate necrosis by enhancing mechanisms leading to hyperemia and mast cell mediators might be involved in the latter effect. Lymphocyte influx and the therapeutic outcome are likely to be related, since exclusively therapeutic treatments reduced the influx of these cells.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed2006

Screening of anti-endotoxin components from Radix isatidis.

To find a component with the strongest anti-endotoxin effect from the four components (F021, F022, F023, and F024) of chloroform extract (F02) of Radix Isatidis, the protective effects of the five components on endotoxin-challenged mice and their effects on the production of TNFalpha and IL-6 by macrophages from the endotoxin-challenged mice were compared. It was found that the five components all had protective effects on endotoxin-challenged mice in terms of mortality. The mortalities of the mice challenged by 2.42 mg/kg endotoxin were 30 %, 50 %, 20 %, 50 % and 60 % after treatment with F02, F021, F022, F023, and F024. The 5 components all had inhibitory effects on the production of TNFalpha and IL-6 by macrophages from the mice. At a concentration of LPS of 50 ng/mL, the inhibitory rates of F02 , F021 1, F022, F023, and F024 for the production of TNFalpha and IL-6 were 76.54 %, 30.86 %, 78.60 %, 36.63 %, 2.06 % and 75.85 %, 18.45 %, 77.68 %, 24.41 %, 3.64% and at the dose of 100 ng/mL, the inhibitory rates were 49.65 Y, 16.86 %, 66.97 %, 13.39 %, 7.16 % and 59.78 %, 1.28 %, 61.86 %, 2.08 %, 1.44 %, respectively. It is concluded that the component F022 of Radix Isatidis has the strongest anti-endotoxin effect.

Animals↗
PubMed2006

Routine clinical laboratory tests correspond to increased serum levels of 3-hydroxy fatty acids, markers of endotoxins, in cardiosurgery patients.

INTRODUCTION: Endotoxemia developing during cardiosurgery as elevated endotoxin concentrations in patient's serum may prevail over 24 h after operation. A major reason is thought to be increased gut permeability resulting in endotoxin and bacterial leakage. In this study we aimed to measure endotoxin levels on samples obtained during and after cardiovascular procedures and compare them with clinical observations and laboratory test results. MATERIALS AND METHODS: 3-Hydroxy fatty acids (3-OH FAs) of 10-18 carbon chain length, chemical markers of endotoxin (lipopolysaccharide), were determined in patient sera by gas chromatography-mass spectrometry-based analysis. RESULTS were compared with routine laboratory tests: blood morphology, urine, ALT, AST, bilirubin, kidney parameters, clotting parameters, and gasometry. RESULTS: Of a total of 16 patients, 5 patients (group I) showed increased serum 3-OH FA levels and 11 patients (group II) did not show any change in 3-OH FA levels 24 h after operation. All group I patients revealed leukocytosis, two developed post-operative anemia. Significantly different changes were observed: the initial, pre-operative 3-OH FA levels were similar for both groups, while group I patients showed increased levels of all the studied 3-OH FAs during the operation (p</=0.05), and 3-OH C14 and 3-OH C16 remained elevated 24 h after the operation. CONCLUSIONS: Cardiosurgery may strongly promote gut endotoxin translocation to the blood in some patients. Prolonged leukocytosis, deep anemia, and increased liver dysfunction markers may indicate the need for observation of possible endotoxemia development. It is recommended to monitor the endotoxin level and/or endotoxemia markers in cardiosurgery patients.

Biomarkers↗
PubMed1999

Eicosanoid release in the endotoxin-primed isolated perfused rat lung and its pharmacological modification.

OBJECTIVE: Recent observations have demonstrated a central role of the "inducible" isoform of the cyclooxygenase (COX), COX-2, in the rat lung. Therefore, the reported capacity of selective COX-2 inhibitors to potentiate the formation of leukotriene (LT) B4 may raise concern about pro-inflammatory side effects of such drugs in the respiratory system. The present study was aimed at determining the effects of the COX-2 inhibitor NS-398 on the release of COX and 5-lipoxygenase (LOX) metabolites of arachidonic acid in isolated perfused lungs obtained from endotoxin-treated rats before and after stimulation with the leukocyte secretagogue N-formyl-methionyl-leucyl-phenylalanine (FMLP). METHODS: Two hours after rats had received endotoxin i.v., the lung was dissected and perfused via the pulmonary artery with physiological salt solution. After an equilibration period of 20 min the outflow was collected (5-min fractions). In the respective treatment groups, indomethacin, NS-398, or the 5-LOX inhibitor MK886 were present throughout the experiment, while FMLP was added to the perfusate during a single 5-min period. The concentration of eicosanoids in the outflow was determined by radioimmunoassay. RESULTS: Endotoxin treatment of rats resulted in increased expression of COX-2 mRNA in lung tissue, and an elevated basal release of the prostaglandin (PG)I2 metabolite 6-keto PGF1alpha, without a detectable increase of leukotriene (LT) formation. In-vitro exposure to FMLP stimulated LT and prostanoid release, which was significantly enhanced in endotoxin-primed lungs, and was suppressed by the 5-LOX inhibitor MK-886 (3 microM) and the COX-inhibitor indomethacin (5 microM), respectively. Either compound showed selective inhibition of the respective pathway of arachidonic acid metabolism. In endotoxin-primed lungs, the COX-2 inhibitor NS-398 (0.3-1.0 microM) depressed basal as well as FMLP-stimulated release of 6-keto PGF1alpha, but did not cause a significant increase of LTB4 or cysteinyl-LT release. CONCLUSIONS: These results suggest that FMLP, presumably acting on inflammatory cells trapped in the pulmonary circulation of endotoxin treated rats, induced prostanoid formation mainly via the COX-2 pathway, and that its inhibition by NS-398 had no detectable potentiating effect on LTB4 or cysteinyl-LT biosynthesis.

6-Ketoprostaglandin F1 alpha↗
PubMed1999

Endotoxin-mediated activation of cytokine production in human PBMCs by collagenase and Ficoll.

Endotoxin-induced early inflammatory reactions may inhibit the function and survival of isolated cells or cell aggregates after transplantation. By the chromogenic Limulus amebocyte lysate assay we found rather high but variable endotoxin concentrations in the chemicals used for islet isolation, i.e. collagenase and Ficoll. Liberase, a special collagenase preparation from Boehringer, was nearly endotoxin-free. Correlating to the endotoxin content, collagenase and Ficoll had the capacity to induce interleukin-1beta release from human peripheral blood mononuclear cells. Because collagenase and density gradient media are needed in most cell isolation procedures from solid organs, each lot of these chemicals should be tested for endotoxin contamination. In pancreatic islet transplantation, the use of endotoxin-free chemicals may diminish early local inflammatory reactions at the graft site and thereby reduce the number of islets needed for successful islet transplantation.

Collagenases↗
PubMed1997

Influence of enoximone on systemic and splanchnic oxygen utilization and endotoxin release following cardiopulmonary bypass.

OBJECTIVE: We investigated whether the administration of enoximone during and after cardiopulmonary bypass (CPB) improves splanchnic oxygen utilization and thereby gut mucosal integrity in humans by its vasodilating and inotropic properties. SETTING: Surgical intensive care unit (ICU) in a university hospital. DESIGN/PATIENTS: 21 patients (ASA III classification) scheduled for elective coronary artery bypass grafting were enrolled in the study. After induction of general anesthesia, patients were randomly assigned to received a bolus of 0.2 mg/kg enoximone, followed by 5 microg/kg per min (enoximone group), or followed by an equal volume of saline (NaCl group) during and 24 h after the surgical procedure. The following parameters were evaluated at different time intervals: systemic and pulmonary hemodynamics, blood gas analysis of arterial, mixed venous, and liver venous blood, venous and liver venous lactate level, venous and liver venous endotoxin level and intramucosal partial pressure of carbon dioxide for calculation of intramucosal pH (pHi). RESULTS: Enoximone raised cardiac output and oxygen delivery to higher levels than those observed in the NaCl group. In both groups, gastric pHi fell continuously during the study period. The values were significantly decreased 12 h following admission to the ICU. Endotoxin was not detectable at baseline. Both groups showed increased endotoxin levels, with the highest values during the first 6 h postoperatively. The hepatic venous endotoxin level was almost doubled in the NaCl group in comparison to the enoximone group. Endotoxin levels differed in the two groups 6 and 12 h after admission to the ICU. CONCLUSIONS: Improvement of oxygen delivery by enoximone did not prevent gastric mucosal acidosis following CPB. However, since the increase in endotoxin levels in liver venous blood was diminished by using enoximone, the drug seems to have a beneficial effect on tissue damage and barrier function of the gut.

Aged↗
PubMed1997

Is endotoxin and cytokine release related to a decrease in gastric intramucosal pH after hemorrhagic shock?

OBJECTIVES: (a) To investigate the relationship between gut ischemia parameters (gastric intramucosal pH [pHi], mucosal-arterial carbon dioxide difference [PCO2-gap]), and endotoxin or cytokine release during hemorrhagic shock; (b) to compare the predictive value of pHi, PCO2-gap and arterial lactate concentrations. DESIGN: Prospective study. SETTING: Surgical intensive care unit of a university hospital. PATIENTS: 20 multiple trauma patients with severe hemorrhagic shock. INTERVENTIONS: Intramucosal measurements and blood samples were obtained on admission to the emergency room and repeatedly over 48 h. MEASUREMENTS AND RESULTS: Endotoxin was measured using a chromogenic limulus amoebocyte assay. Cytokine [tumor necrosis factor-alpha (TNF alpha) and interleukin-6 (IL-6)] values were evaluated by immunoradiometric assays. Only 3 patients had positive blood cultures but endotoxins were detected at least once in all patients. Endotoxin levels were similar in survivors and non-survivors over the study period and were not related to pHi or PCO2-gap. Initially, high levels of IL-6 were observed in both nonsurvivors and survivors [median 1778 pg/ml (range 435-44,540) vs 2068 pg/ml (range 996-92,300)]. IL-6 levels progressively decreased in the survivors but not significantly. On admission, TNF alpha concentrations were similar in nonsurvivors and survivors (42 +/- 35 vs 46 +/- 27 pg/ml). From the 24th h, TNF alpha values were higher in the nonsurvivors than in the survivors (24 h: 72 +/- 38 vs 34 +/- 17 pg/ml, p < 0.05). The greatest IL-6 levels were found for a pHi < 7.20 (28.5 +/- 36.5 vs 1.8 +/- 1.3 ng/ml, p < 0.05) or a PCO2-gap > 7.5 mmHg (1 kPa) (32.5 +/- 37.5 vs 1.7 +/- 1.3 ng/ml, p < 0.01). With the same pHi threshold, no difference was found in endotoxin levels. The lactate concentrations were predictive for outcome from the 12th h (9.5 +/- 5.9 vs 3.6 +/- 2.3 mmol/l, p < 0.05). CONCLUSIONS: During severe hemorrhagic shock, endotoxin translocation from the gut was a common phenomenon that seemed independent of both pHi values and outcome. It could not explain IL-6 and TNF alpha release. In severe hemorrhagic shock, neither pHi nor PCO2-gap provides additional information to the lactate measurements.

Adult↗