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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The continuous infusion of E. coli lipopolysaccharide (100 mg/kg in 4 h) caused a 100%-mortality in pentobarbital-anesthetized rats within 6 h. Recombinant human superoxide dismutase (r-HSOD) infused concomitantly with the E. coli endotoxin dose-dependently (0.1-1.0 mg/kg per min) increased survival rate up to 90%. Significant improvement of survival rate was also obtained when r-HSOD-infusion (0.464 mg/kg per min) was only started up to 3 h after beginning of the endotoxin application. Also, two single bolus injections of r-HSOD (20 mg/kg each) during endotoxemia significantly increased survival rate. Decrease of heart rate was prevented and decline of arterial blood pressure was diminished by r-HSOD (0.464 mg/kg per min) as compared to vehicle-treated endotoxemic rats. Lactic acidosis occurred with no significant statistical difference between r-HSOD- and vehicle-treated groups. Increase of hematocrit in endotoxemic control rats was balanced by fluid uptake. In contrast, in the groups treated with endotoxin plus r-HSOD or saline alone hematocrit decreased identically. Decrease of whole blood leukocytes (to 30.2 +/- 9.5% of baseline in endotoxemic controls) was less pronounced in the r-HSOD group (fall to 49.2 +/- 6.5% of baseline), but this difference did not reach statistical significance. Marked thrombocytopenia (to 12.9 +/- 3.2% of baseline) and consumption of plasma fibrinogen (to 39.5 +/- 10.3% of baseline) were significantly attenuated in r-HSOD-treated rats, where thrombocytes only decreased to 28.1 +/- 3.6% and plasma fibrinogen to 76.6 +/- 5.0% of baseline values at the end of endotoxin infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prophylactic and curative effects of recombinant human superoxide dismutase in lethal rat endotoxemia. 306 66

Cyanoginosin-LR, one of the group of virulent cyclic heptapeptide toxins (cyanoginosins) isolated from some strains of the cyanobacterium, Microcystis aeruginosa, kills mice within 1-2 hr after iv or ip injection. Although the liver is a target organ of the toxin, the rapidity of lethality is incompatible with metabolic death from failure of hepatocellular function. However, disintegration of sinusoidal endothelium causes massive intrahepatic hemorrhage. The loss of the structural integrity of hepatic sinusoids provides a previously undescribed mechanism for embolization of disintegrating cells from the liver to the lung. No injury to either cultured bovine pulmonary artery endothelial cells or mouse peritoneal macrophages was observed following prolonged incubation with high concentrations of the toxin, and there was no increase in vascular permeability to 125I-labeled albumin detected before intrahepatic hemorrhage. However, plasma fibronectin increased transiently after toxin injection. Acute, severe thrombocytopenia, a characteristic of cyanoginosin-LR toxicity, remains unexplained since platelets did not concentrate in the lungs, liver, or spleen. There are similarities between the effects of cyanoginosin-LR and of the lipopolysaccharide endotoxins, such as elevations of plasma levels of thromboxane B2 and 6-keto-prostaglandin F1 alpha.
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PMID:Pathophysiology of cyanoginosin-LR: in vivo and in vitro studies. 319 14

Experimental thrombosis which developed exclusively in glomerular capillary walls was induced in rats by the combined injection of nephrotoxic antiserum (0.2 ml of pooled material) as a preparatory agent and 20 micrograms or more of lipopolysaccharide as a provoking agent. Effects of some antiplatelet and anticoagulant drugs on the glomerular lesions were tested in this experimental glomerular thrombosis. With administration of 2000 units/kg or more of heparin at the time of provoking injection, coagulation time was prolonged for over 5 hr, and the glomerular thrombosis was adequately prevented. Prolongation of prothrombin time (PT) for over 60 sec to prevent thrombosis required warfarin, but with this drug there was only a narrow margin between an effective dose and that which produced a fatal hemorrhage. Low levels of fibrinogen (less than 50 mg/dl) induced by batroxobin seemed to protect partially and high doses of urokinase did not seem to protect from glomerular thrombosis. OP-41483, a derivative of prostacyclin which is about five times more active than PGE1 in inhibiting platelet aggregation, and other anti-platelet drugs except for ticlopidine were not effective in preventing glomerular thrombosis. These findings were in accordance with the fact that thrombocytopenia induced by antiplatelet antiserum did not prevent glomerular thrombosis. Ticlopidine may have a unique and valuable therapeutic potential for the control of this condition.
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PMID:Effect of drug administration on experimental renal glomerular thrombosis. 328 90

Thrombocytopoiesis was evaluated in T cell-deficient nu/nu mice and in T cell-replete nu/+ controls to determine if abnormalities would be associated with the deficiency of T cells. Mice were studied in the unperturbed steady state and after acute immunothrombocytopenia was induced by an injection of guinea pig antimouse platelet serum (APS). The state of thrombocytopoiesis was determined from platelet counts, megakaryocyte size, megakaryocyte number, and numbers of Meg-CFC. Splenic lymphocytes were evaluated by response to the mitogens bacterial lipopolysaccharide (LPS), phytohemagglutinin (PHA), and concanavalin A (Con A). Hematocrits, reticulocyte counts, leukocyte counts, marrow cellularity, GM-CFC, and BFU-E also were measured. Steady state thrombocytopoiesis was identical in nu/nu and nu/+ mice. In response to an injection of APS, acute thrombocytopenia was followed by macromegakaryocytosis and rebound thrombocytosis in mice of both genotypes. Splenic Meg-CFC increased in nude mice after APS or an injection of normal guinea pig serum (NGpS), and splenic GM-CFC increased after APS. Neither Meg-CFC nor GM-CFC increased in the spleens of nu/+ mice, but they showed early transient increases in bone marrow that did not occur in nu/nu mice. Sporadic, but weak, mitogenic responses to PHA or Con A were occasionally observed with nu/nu spleen cells, but these did not correlate with the state of thrombocytopoiesis. The results demonstrated that platelet production was normal in nu/nu mice and that megakaryocytopoiesis and platelet production responded to the stimulus imposed by acute immunothrombocytopenia. Increases in megakaryocyte size and platelet production occurred independently of changes in numbers of Meg-CFC, GM-CFC, or BFU-E. A normal complement of T cells appears to be unnecessary for normal platelet production and its augmentation in response to the stimulus of acute immunothrombocytopenia in vivo.
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PMID:Thrombocytopoietic response to immunothrombocytopenia in nude mice. 349 39

Immune responses and hematologic alterations were investigated in splenectomized pigs after IM inoculation with Eperythrozoon suis. Early hematologic alterations were massive parasitism of RBC, severe hypoglycemia, moderate bilirubinemia, and mild anemia; later findings included severe anemia, minimal parasitism of RBC, spontaneous agglutination of RBC at 25 C and 4 C which was reversible at 37 C, transient thrombocytopenia, and mild bilirubinemia. The humoral immune responses consisting of a transitory hyperglobulinemia and increase of indirect hemagglutination (IHA) titers against E suis were attributed to immunoglobulin M cold agglutinins. Cell-mediated immune responses, measured by phytohemagglutinin- and pokeweed mitogen-induced lymphocyte blastogenesis, were reduced after massive parasitemia. Blastogenesis induced by Escherichia coli lipopolysaccharide mitogen was increased before the hyperglobulinemia and an increase in IHA titer. There was an increase in the uptake of [3H]thymidine by lymphocytes cultured without mitogens after the decline in total globulin concentration and IHA titer.
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PMID:Experimental porcine eperythrozoonosis: T-lymphocyte suppression and misdirected immune responses. 387 72

An early hypotensive phase was induced in rats by different strains of Escherichia coli and cell wall fractions to study the role of the bacterial surface structure, the complement system, histamine, and serotonin in induction of hypotension. E. coli strains with only core glycolipid (E. coli strain J5) or with intact lipopolysaccharide O antigens on their surface induced hypotension and thrombopenia within 5 min after intravenous administration. This response was reduced by prior decomplementation of the rats and by methysergide, a serotonin antagonist. Two K antigen-positive strains induced no hypotension except after removal of K antigen. The isolated lipopolysaccharide fractions and the lipid A subfractions, but not the polysaccharide subfractions, were also able to induce hypotension. Thus the core glycolipid structure, by interactions that involve platelets and the complement system, is mainly responsible for induction of an early hypotensive phase in rats, and K antigens interfere with this response.
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PMID:Induction of the early hypotensive phase by Escherichia coli: role of bacterial surface structures and inflammatory mediators. 389 97

Pertussis vaccine contains lipopolysaccharide (endotoxin). Polymyxin B sulfate neutralizes endotoxin activity in vivo and in vitro from Enterobacteriaceae and Salmonella-derived endotoxin. In vitro, polymyxin B eliminates the endotoxin reaction of pertussis vaccine in the Limulus lysate test. In this study, platelet and WBC counts and antibody response were compared in rabbits given either pertussis vaccine alone or pertussis vaccine and polymyxin B intravenously. Pertussis vaccine-induced leukopenia and thrombocytopenia were eliminated in the polymyxin B group. The antibody titers in the animals receiving pertussis vaccine and polymyxin B were somewhat lower and rose more slowly. Since the toxicity of pertussis vaccine is related in part to endotoxin, we suggest that a clinical study using a combination of the vaccine with an endotoxin-neutralizing agent be done to assess both amelioration of side effects caused by the vaccine and any effect on immunogenesis.
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PMID:In vivo effect of polymyxin B on pertussis vaccine. 632 72

Severe infections and particularly infectious shock are frequently accompanied by a varying degrees of disseminated intra-vascular coagulation (DIC). The mechanism at work is complex, involving endotoxin or bacterial lipopolysaccharide constituents that damage vascular endothelium and activate intrinsic coagulation, platelet function and the release of leucocyte coagulation-promoting compounds. The activation of coagulation in turn activates prekallikrein and complement and plays a part in shock. The laboratory plays an essential role in diagnosing DIC, determining its repercussions on the parameters of haemostasis and in monitoring its course under antibiotics, which in some cases may be combined with carefully controlled heparin treatment. Sensitive and specific tests are the assays for fibrinogen-fibrin degradation products (FDP) and soluble complexes (SC) using the haemagglutination test or the ethanol test. The platelet count should be combined with measurement of the bleeding time. A varying degree of thrombopenia is frequent but non specific. In cases of septicemia, it is an early warning sign. A selective fall in proaccelerin is an indirect early sign. A fall in antithrombin III (AT III) is considered a good sign of DIC but it does not occur in every case, and is most liable to be present in liver failure. From the FDP and fibrinogen results, it should be clear whether one is dealing with compensated, decompensated or even over-compensated DIC. Diagnosis should be complemented by a careful search for the clinical signs of coagulation and haemorrhage. It is indispensable for investigations to be repeated every 6-12 hours, for the sake both of treatment strategy, which can be extremely difficult, and DIC monitoring.
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PMID:[Diagnosis of defibrination syndromes in infectious pathology]. 673 53

Administration of endotoxin (lipopolysaccharide W E. coli O111 B4, 0.5 mg/kg i.v.) induced about 20% activation of the complement system (measured as CH50 and C3), a biphasic hypotension, thrombocytopenia and a significant rise in blood levels of 6-oxo-PGF1 alpha. Complement depletion (CH50 and C3 less than 3%) with Cobra Venom Factor significantly reduced the initial fall in blood pressure and the rise in 6-oxo-PGF1 alpha, and abolished the second phase of hypotension and the thrombocytopenia, due to subsequent injection of endotoxin. It is concluded that activation of about 20% of the complement system by endotoxin is a prerequisite for the occurrence of thrombocytopenia and secondary hypotension, and that it is involved in the increase in blood levels of 6-oxo-PGF1 alpha. The results of histamine determinations in rabbit blood and plasma indicate that, besides products derived from prostaglandin endoperoxides, other vasoactive substances, possibly released during complement-mediated adherence aggregation of platelets, might contribute to the endotoxin-induced hypotension.
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PMID:Contribution of complement activation to the rise in blood levels of 6-oxo-prostaglandin F1 alpha during endotoxin-induced hypotension in rabbits. 689 7

Treatment of experimental murine borreliosis induced an acute transient fall in temperature, leucopenia and thrombocytopenia with appearance of circulating 'endotroxin-like' material. This reaction to treatment could be reproduced by the inoculatioh of borrelial sonicates into infected mice or by two injections of the same sonicate given 24 hours apart, into normal mice. Sensitization or precipitation of the reaction could not be induced by E. coli lipopolysaccharide, although a reaction indistinguishable from the reaction to treatment could be provoked in mice by two successive injections of lipopolysaccharide given 24 hours apart. The nature of this reaction in mice was investigated and the relation of both reactions to the Shwartzman reaction, Endotoxin.
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PMID:Reaction following treatment of murine borreliosis and Shwartzman type reacion with borrelial sonicates. 741 46


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