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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 role of fibrin in the pathogenesis of renal glomerular scarring in the dog was studied. Fibrin deposition, resulting from disseminated intravascular coagulation, was induced by intravenous injection of Liquoid (sodium polyanethol sulphonate). Thirty-eight puppies were killed from 30 minutes to 39 days after treatment, and the renal lesions examined by light, electron and immunofluorescence microscopy. The major acute lesions in the glomeruli were capillary thrombosis, mesangial and endothelial cell swelling and phagocytosis of fibrin, polymorphonuclear leukocyte infiltration and necrosis. Animals that recovered from this acute phase had focal glomerular scars. Affected glomeruli showed combinations of mesangial enlargement, focal tuft hypercellularity, collagen formation, thickening, wrinkling and duplication of the glomerular basement membranes, and some capsular adhesions. These observations indicate that fibrin deposition can be an important mechanism in glomerular scarring in the dog.
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PMID:Liquoid-induced renal lesions in the dog. 625 82

Fibrin clots have been detected at sites of inflammation, and kinins have been implicated as mediators of the vascular phenomena of acute inflammation, systemic shock, and disseminated intravascular coagulation. It is now reported that both negatively and positively charged asbestos fibers shorten the partial thromboplastin time of human plasma, indicating coagulation of the plasma. A sample containing short (less than 5 micron in length) chrysotile fibers is ineffective. Only the negatively charged amphiboles (crocidolite and amosite) are able to activate factor XII (Hageman factor). This particular effect of the amphiboles is enhanced by high molecular weight kininogen and leads to kinin formation.
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PMID:Asbestos fibers, plasma and inflammation. 664 59

Figure 5 summarizes the three different phases in the pathophysiology of disseminated intravascular coagulation exemplified by the effect of endotoxin. During the first phase, the coagulation system is activated to generate soluble fibrin. Fibrin kept in solution by fibrinogen or fibrinolytic degradation products can be cleared from the circulating blood. If the amount of soluble fibrin exceeds a certain threshold, soluble fibrin may precipitate or polymerize to fibrin clots. At this state, active fibrinolysis breaks down the precipitated fibrin to fibrinolytic degradation products preventing the preservation of fibrin. If the capacity of the fibrinolytic system is exhausted, or if fibrinolysis is inhibited, fibrin clots may be preserved, causing cell damage, as for instance bilateral renal cortical necrosis.
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PMID:Pathogenesis of disseminated intravascular coagulation. 666 51

Extensive gangrene of both lower extremities necessitating bilateral above-the-knee amputations complicated the adult respiratory distress syndrome (ARDS) caused by Escherichia coli pneumonia and septicemia in a 52-yr-old man. Concurrent with the evolution of tissue necrosis, peripheral blood leukocyte and platelet counts fell, and pulmonary vascular resistance increased. Adequacy of the cardiac output was confirmed by repeated thermodilution cardiac output measurements, and major vascular occlusion was excluded surgically. Fibrin degradation products and thrombocytopenia were present, but the other usual criteria for disseminated intravascular coagulation were absent. Small vessel thrombosis by fibrin and leukocytes was observed histologically in the amputated extremities. These findings suggest that gangrene was due to the "microembolism syndrome"--diffuse small vessel occlusion by fibrin thrombi complicating ARDS. This unusual complication of ARDS may occur without abnormalities suggestive of diffuse intravascular coagulation in routine laboratory tests of blood coagulation. It should be suspected and treated promptly to avoid severe disability in survivors.
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PMID:Ischemic necrosis of both lower extremities as a result of the microembolism syndrome complicating the adult respiratory distress syndrome caused by Escherichia coli pneumonia and septicemia. 675 35

Disseminated intravascular coagulation (DIC) is a common occurrence during clinical sepsis and can be induced in the experimental host by LPS. Fibrin deposition in the hepatic microcirculation has been observed within 30 min of i.v. injection of LPS. Because mononuclear phagocytes have been shown to produce a PCA after exposure to LPS, we have examined the ability of a homogeneous population of explanted hepatic macrophages to express PCA. Addition of as little as 10 ng/ml of LPS stimulated a 15- to 20-fold increase in PCA over control culture levels within 7 1/2 hr post-treatment. The PCA was found to be membrane-associated, with approximately 90 to 95% of the total PCA present in the cellular lysates, and more than 85% was inhibited by pretreatment of the cells with the diazonium salt of sulfanilic acid, an inhibitor of ecto-enzymes. In contrast to tissue thromboplastin produced by other M phi populations, the H-M phi PCA was found to be markedly sensitive both to heat inactivation at 56 degrees C and to inhibition by 1 mM DFP. Additionally, assays involving both a 1-stage coagulation test as well as an enzyme assay with a Factor Xa-specific substrate (using normal and deficient human plasmas) demonstrated that the H-M phi PCA appears to activate Factor X directly. Unlike tissue thromboplastin, the H-M phi PCA is non-dependent of Factor VII activation. These studies: 1) demonstrate the LPS induces a unique PCA in the H-M phi, and 2) support a role for the H-M phi in the initiation of DIC in endotoxemic shock.
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PMID:The induction of a unique procoagulant activity in rabbit hepatic macrophages by bacterial lipopolysaccharides. 702 10

Weanling male rats fed on a hypolipotropic diet develop acute renal failure whose morphological features vary from focal tubular necrosis to cortical necrosis. We have sequentially studied the hemostatic mechanism in correlation with the morphology of various tissues, mainly renal and hepatic, in choline-deficient rats as well as in three control groups. No important changes were observed in the hemostatic mechanisms before the development of tubular necrosis. Along with tubular necrosis a consumption coagulopathy was found, evidenced mainly by a decrease in the activity of factors V and VIII as well as a prolongation in PTTK and Quick's time and a decrease in platelets. Fibrin degradation products were found in serum and urine and soluble fibrin monomer complexes in the former. Following tubular necrosis thrombi were found in the renal microvasculature. It is possible to speculate that the tubular necrosis induced by choline deficiency could produce an activation of the coagulation system which in turn would lead to thrombosis of the renal microcirculation and cortical necrosis.
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PMID:Consumption coagulopathy in acute renal failure induced by hypolipotropic diets. 731 82

Polyethylene glycol(PEG) was used to precipitate fibrinogen to prepare defibrinated plasma in the two stage clotting assay of antithrombin activity. Five percent PEG-8000 precipitated fibrinogen from plasma without loss of antithrombin activity in the defibrinated plasma. Fibrin degradation products(FDP) as high as 640 ug/ml did not interfere the two stage clotting assay using PEG defibrinated plasma possibly because part of FDP was precipitated by PEG in the process of plasma defibrination. The two stage clotting assay was very sensitive to the changes of antithrombin activity in the range of 60%-100% of normal level. The assay was reproducible and correlated with chromogenic assay. The decrease of plasma antithrombin activity in a baboon septic shock model was demonstrated with this assay.
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PMID:Functional assay of plasma antithrombin using polyethylene glycol (PEG) defibrinated plasma. 748 43

The purpose of this pilot study was to determine the effect of recombinant hirudin (r-hirudin) on coagulopathy and the relationship between concentrations of thrombin-antithrombin III (ATIII) complex (TAT) and thrombin-hirudin complex (THC) in patients with disseminated intravascular coagulation (DIC). Five patients with haematological malignancy associated with DIC were studied. r-Hirudin was administered by continuous intravenous infusion at a dose of 0.005 mg/kg/h for 4-9 days to each patient. Fibrin/fibrinogen degradation products (FDP), D-dimer, TAT and plasmin-alpha 2 antiplasmin complex (PAP) concentrations decreased after treatment with r-hirudin in four patients studied. However, in one patient, serum creatinine increased to 1.7 mg/dl and aPTT was prolonged to 74.4s. Statistical analysis disclosed significant positive correlations between plasma concentrations of hirudin and THC, and between concentrations of THC and TAT. The concentrations of THC were much higher than those of TAT. In conclusion, these findings indicate that r-hirudin more strongly inhibited thrombin than did ATIII without heparin, and that administration of r-hirudin to renal insufficiency required individual adjustment of dosage. The present findings also suggest that r-hirudin can be considered a new agent for the treatment of DIC.
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PMID:Recombinant hirudin for the treatment of disseminated intravascular coagulation in patients with haematological malignancy. 754 Aug 78

Dysbaric osteonecrosis (DON) can occur in humans and sheep after a single hyperbaric air exposure with inadequate decompression. The authors hypothesize that DON does not result from primary embolic or compressive effects of nitrogen bubbles on the osseous vasculature, but by secondary injury to the marrow adipose tissue by rapidly expanding nitrogen gas that triggers local, and possibly systemic, intravascular coagulation. A 28-year-old scallop diver remained at a depth of 92 feet in sea water for 4.5 hours on surface-supplied compressed air. Decompression sickness occurred after a no-stop ascent to the surface, and he died 70 minutes later. Autopsy showed multiple gas bubbles, not only within the great vessels, but in the fatty marrow of his femoral and humeral heads. Lipid and platelet aggregates were found on the surface of marrow bubbles. Fibrin-platelet thrombi were detected within dilated venous sinusoids adjacent to bubbles, and in veins, capillaries, and arterioles. Since pulmonary, renal, and intraosseous (subchondral) fat embolism and fibrin thromboses were observed, it is suggested that injured marrow adipocytes can release liquid fat, thromboplastin, and other vasoactive substances, which conceivably can also play a systemic procoagulant role in triggering disseminated intravascular coagulation and additional DON.
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PMID:The pathophysiologic role of fat in dysbaric osteonecrosis. 822 35

The bone marrow of a 53-year-old woman with acute myeloid leukemia (AML) with disseminated intravascular coagulation was investigated by transmission electron microscopy. The patient had a preceding granulocytic sarcoma, and subclinical disseminated intravascular coagulation occurred concomitantly with the development of AML. Ultrastructural findings of the bone marrow at the onset of AML revealed the following: (1) The cytoplasm of the leukemic cells showed frequent fragmentation, resulting in the formation of abundant cytoplasmic fragments. (2) These cytoplasmic fragments were surrounded by abundant fibrin fibers, forming the fibrin-cytoplasmic fragment complex (FCF complex). (3) Slight fibrin deposition was seen around the leukemic cells and in the intercellular space of the bone marrow. Fibrin deposition in the bone marrow is thought to represent morphologic evidence of disseminated intravascular coagulation. The damage on the leukemic cell surface due to the cytoplasmic fragmentation seems to be closely related to the development of disseminated intravascular coagulation.
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PMID:Disseminated intravascular coagulation in a patient with acute myeloid leukemia. Ultrastructural evidence of hypercoagulation in bone marrow. 832 4


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