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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results of a study conducted to determine the clinico-pathological changes in 4 experimentally-induced cases of endotoxaemia in the horse are reported on. Endotoxaemia was induced by injecting commercially available E. coli 055:B5 lipopolysaccharide intravenously at a dose of 1 microgram kg-1. The haematocrit, red cell count, total and differential white cell counts, thrombocyte count, prothrombin time, partial thromboplastin time, fibrinogen level, level of fibrin degradation products, arterial acid-base status, serum lactate and blood glucose were determined repeatedly. Changes that occurred, include increases in the haematocrit and red cell count, a leucopaenia followed by a leucocytosis caused mainly by changes in the number of neutrophils, the development of disseminated intravascular coagulation, minor changes in the arterial acid base parameters, hyperglycaemia followed by hypoglycaemia and an increase in serum lactate.
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PMID:[Clinico-pathological changes after intravenous administration of endotoxin in the horse]. 248 30

We have evaluated the quantitative relationship between lipopolysaccharide (LPS, endotoxin), fibrinopeptide A (FPA), antithrombin (AT), protein C (PC) and extrinsic pathway inhibitor (EPI) in plasma from 39 consecutively admitted patients with systemic meningococcal disease (SMD). The most severely ill patients with fulminant meningococcal septicemia (n = 13, 6 dead) had significantly (p less than 0.01) higher plasma levels of LPS and FPA and lower levels of PC and AT on admission as compared with the less severe clinical presentations (n = 26, 1 dead). The levels of EPI on admission were significantly (p less than 0.05) higher in nonsurvivors vs survivors with fulminant septicemia. As the disease progressed, the levels of LPS, FPA, AT and PC declined, while the levels of EPI increased. Three of six nonsurviving septicemic patients had levels of EPI greater than 200% within 16 hours of admission vs two of 30 survivors (p = 0.02). The results suggest that increasing levels of LPS in SMD elicit increasing consumption coagulopathy, contributing to the organ pathophysiology. The kinetics of EPI, inhibiting the thromboplastin-FVIIa-FXa complex, differs markedly from the kinetics of AT and PC i.e. increases as opposed to decreases.
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PMID:The quantitative association of plasma endotoxin, antithrombin, protein C, extrinsic pathway inhibitor and fibrinopeptide A in systemic meningococcal disease. 251 Mar 54

Analysis of fatal sensitivity to 0.2 microgram of S. enteritidis lipopolysaccharide in cycloheximide-treated mice identified two independent lethal elements. First, an absolute requirement for steroid supplementation to ensure survival suggests a crucial role for cycloheximide-mediated inhibition of steroidogenesis. The second factor is the development of virtually total bilateral renal cortical necrosis, itself a consequence of glomerular capillary occlusion with fibrin-like material. The survival of cycloheximide and endotoxin-challenged mice requires both hydrocortisone treatment and defibrination with ancrod. Cycloheximide and a smaller dose of endotoxin (0.1 microgram per mouse) is also fatal, but here steroid deficiency is not a crucial factor, protection being conferred by ancrod defibrination alone.
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PMID:Factors involved in the fatal susceptibility to submicrogram doses of endotoxin in cycloheximide-treated mice. 264 18

Endotoxins (lipopolysaccharides, LPS) are potent bacterial poisons always present within the intestines in considerable amounts. Several pathophysiological conditions such as hypovolaemia, hypoxia, intestinal ischaemia, burns and radiation lead to a breakdown in the barrier and depending upon the extent of the injury, endotoxins enter the systemic circulation in increasing amounts. Antibiotics do not inactivate the endotoxins which continue to exert their toxic effects leading to nausea, vomiting, diarrhoea, fever, disseminated intravascular coagulation, vascular collapse and organ failure. When nonabsorbable antibiotics are given prior to the insult, systemic endotoxaemia is prevented. Immunotherapy, using anti-lipopolysaccharide IgG, inactivates plasma endotoxins, destroys gram-negative bacteria and opsonises them and may become a major form of therapy. An outline of endotoxin and anti-lipopolysaccharide and its importance to the anaesthetist and intensive care specialist is presented.
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PMID:Endotoxins and anti-endotoxins (their relevance to the anaesthetist and the intensive care specialist). 265 93

To clarify the initiation, development and recovery processes of disseminated intravascular coagulation (DIC), rat glomerular capillaries and fibrin thrombi were examined under transmission and scanning electron microscopes. DIC was induced in rats by a single intraperitoneal injection of endotoxin (Et., 7.5 mg/kg lipopolysaccharide:B, E. coli 026:B6). At 2 h after Et. injection, the endothelial surface of the glomerular capillary became irregular with projections like a sea anemone. At 4 h after Et. injection, agglomerated fibrin thrombi composed of fibrin fiber bundles with fine cross-striated fibriform structures were observed in the capillary lumen. The fibrin thrombi gradually changed into fine reticular systems suggesting a degradation process by 6 h after Et. injection, and formed a coarse granular agglomerate by 8 h after Et. injection. These fibrin thrombi disappeared within 12 h of Et. injection, but the endothelial surface remained edematous. At 24 h after Et. injection, the microstructure of the glomerular capillaries returned normal. Based on these observations, we concluded that DIC was primarily initiated by injury to the capillary endothelium, and that changes on the endothelial surface contributed to the development of DIC.
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PMID:Initiation and recovery processes of endotoxin induced disseminated intravascular coagulation (DIC): scanning and transmission electron microscopic observations of rat renal tissues. 272 5

We previously reported that calcium entry blockers (CEBs) protected against endotoxin-induced mortality in rats. In this investigation, the i.v. injection of endotoxin (ETX) in control awake male Wistar rats was found to produce pathophysiological changes indicative of disseminated intravascular coagulation (DIC). The latter included increased serum fibrin (ogen) degradation products (FDP), decreased plasma fibrinogen, reduced blood platelet count as well as microscopic findings of fibrin microthrombi in small blood vessels of visceral organs. Gross pathological examination revealed pronounced hemorrhagic congestion of the gastrointestinal tract and petechial and ecchymotic hemorrhages in other visceral organs. Pretreatment with the CEBs, nilvadipine (FR 34235) and nitrendipine, inhibited the elevation in serum FDP and decrease in plasma fibrinogen but did not prevent the thrombocytopenia produced by ETX. The gross pathological manifestations of DIC were also inhibited by pretreatment with the CEBs. The results suggest that the protective effect of CEBs against endotoxin-induced mortality in rats may be related to inhibition of DIC caused by the lipopolysaccharide.
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PMID:The effects of the calcium entry blockers, nilvadipine and nitrendipine, on endotoxin-induced disseminated intravascular coagulation. 279 86

Tissue factor is a lipoprotein, expressed on the surface of cells, which binds coagulation Factor VII or VIIa, leading to activation of Factors X and IX with subsequent fibrin generation. Cellular tissue factor activity is important in pathophysiologic processes such as inflammation and disseminated intravascular coagulation. In this study, the long-chain base sphingosine inhibited coagulation initiated by lipopolysaccharide-stimulated intact human monocytes. Sphingosine (5-100 microM) also profoundly inhibited thromboplastin-initiated coagulation (greater than 90% decrease in thromboplastin activity). This inhibition was dose- and time-dependent. Sphingosine inhibited neither the intrinsic pathway of coagulation nor thrombin generation of fibrin. The sphingosine analogues sphingomyelin, ceramide, or N-acetylsphingosine did not affect thromboplastin activity, suggesting that the polar head of sphingosine was necessary for interaction of the molecule with the coagulation system. Investigation of the biochemical mechanism revealed that sphingosine (5-50 microM), but neither sphingomyelin nor ceramide, inhibited specific binding of radiolabeled Factor VII to lipopolysaccharide-stimulated intact monocytes. The results suggest that sphingosine may regulate monocyte tissue factor-initiated coagulation by modulating Factor VII binding to tissue factor. Sphingosine may represent a new class of inhibitors of hemostasis.
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PMID:Sphingosine inhibits monocyte tissue factor-initiated coagulation by altering factor VII binding. 280 83

The DIC model (Duodenal Inoculation with ligation of the Cecum in rabbits) was employed to study experimentally induced cholera and the related protective immunity. Duodenal inoculation (DI) without ligation of the cecum with live V. cholerae organisms did not cause any disease symptom but induced protection against subsequent challenges with homologous and heterologous organisms for up to 24 months. After 30 months this protective immunity began to decrease. A similar protective immunity could be induced by administration of the A- B+ derivative CVD101 of V. cholerae strain 395. This type of experiment can only be done successfully with conventional, healthy rabbits held under low stress conditions. A so-called specific pathogen-free rabbit breed was found to be entirely unsuitable. Duodenal inoculation with heat- or merthiolate-inactivated V. cholerae for a prolonged period of time by means of an intestinal osmotic minipump did not induce protection. Injection of heat-inactivated V. cholerae material into the Peyer's patches sometimes led to protection, suggesting that a thermostable antigen, possibly lipopolysaccharide, is one of the major protective antigens. Duodenal administration of a combination of inactivated V. cholerae serotypes Ogawa and Inaba cells and 1 mg B subunit of the V. cholerae enterotoxin by up to three inoculations protected only 3 out of 12 rabbits against challenge. The results obtained on the rabbit model are discussed in relation to the efficacy of this vaccine in human volunteers and in a recent field test.
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PMID:Protective immunity against Vibrio cholerae infection in the rabbit. 296 58

The Shwartzman reaction is a classic biologic response in which the coagulation system is activated in vivo. Cellular initiation of the extrinsic coagulation protease cascade can be mediated by one or more limbs of the lymphoid response to diverse biological stimuli. The T cell-instructed monocyte and macrophage responses that have been implicated are mediated by a number of different cellular pathways and are elicited not only by antigens and allogeneic cells but also by other stimuli such as immune complexes and the lipid A moiety of bacterial lipopolysaccharide (LPS). The latter response has been implicated in the pathogenesis of the disseminated intravascular coagulation associated with bacterial infection. In the rapid collaborative cellular pathway response to LPS, we have described a relatively rigorous requirement for T helper cells in induction of the biosynthesis of tissue factor and Factor VII by monocytes. To elucidate potential regulatory aspects of this cellular procoagulant response, we provide the first evidence for the existence of T suppressor cells for the cellular procoagulant response to LPS by the rapid T cell-instructed pathway. Human peripheral blood lymphocytes were separated by cytoaffinity into Fc gamma-positive and Fc mu-positive cells and were characterized for their functional properties in the procoagulant response. T mu cells mediated the monocyte response, consistent with their identity with instructor cells. T gamma cells suppressed the response of monocytes to LPS in the presence of T mu cells, suggesting that they possess suppressor function for this response. The T gamma suppressor cells required stimulation by LPS to express their suppressor function and they exerted their suppressive effect directly on the monocyte. The existence and participation of LPS-responsive T suppressor cells on the cellular procoagulant response in vitro add a new dimension to the complexity of the rapid pathway of the collaborative cellular procoagulant response and may be important in the pathogenesis of disseminated intravascular coagulation.
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PMID:Regulatory roles of T mu and T gamma cells in the collaborative cellular initiation of the extrinsic coagulation pathway by bacterial lipopolysaccharide. 316 8

Cholera disease can be induced in the rabbit by ligation of the cecum (C) followed by duodenal inoculation (DI) of virulent Vibrio cholerae organisms (DIC model). When the cecum is not ligated, DI does not induce disease. In contrast, the animals are primed which becomes apparent upon challenge with live V. cholerae in the DIC model. Such animals are vibriocidally protected. This protection is characterized by absence of disease symptoms, rapid disappearance of V. cholerae from the feces and presence of high levels of anti-lipopolysaccharide Immunoglobulin A in the bile. The present study shows that primed rabbits can also be boosted by duodenal administration of killed, smooth V. cholerae cells. On the other hand, killed cells cannot prime. The minimal lethal dose of a rough derivative of a smooth strain C5, designated R5 and lacking the O antigen part of the LPS, was 100,000 times higher than that of its parent strain C5, in the DIC model. Rabbits which had been duodenally immunized with strain R5 and were subsequently challenged with the smooth strain C5, all developed diarrhea and two out of eight died. This result supports an earlier observation that the specific O antigen part of the V. cholerae LPS is an essential prerequisite for the induction of protective immunity in the rabbit.
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PMID:Priming and boosting of the rabbit intestinal immune system with live and killed, smooth and rough Vibrio cholerae cells. 320 Jan 61


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