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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 blood and liver giver animals are given "Tromexan" for a period of three days. The blood defibrination is finished off by shaking. The perfusion is made of defibrinated blood to which is added a compounding of mineral salts, albumin and glucose in adequate proportions. The fluid is used during 150 minutes with a biliary flow of 4 ul/minute (instead of 8 in perfusions with heparine). The validity of the preparation is tested by biliary acids, cholesterol and Brom Sulfon Phtalein biliary elimination research. This fluid can be used when heparin is avoided: for example in a case of investigation of fat emulsion scrubbing.
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PMID:[Perfusion of isolated rat liver. Utilization of a perfusion without heparin. Validity of the preparation]. 14 84

Consumption coagulopathy and microangiopathic hemolytic anemia occurred as a complication of insertion of an axillofemoral, preclotted dacron graft. Treatment with heparin followed by dipyridamole and aspirin normalized the hematologic and coagulation abnormalities over a two month period. The mechanism of consumption coagulopathy associated with prosthetic grafts is discussed and a possible role for treatment with antiplatelet agents is suggested.
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PMID:Consumption coagulopathy and microangiopathic hemolytic anemia with an axillo-femoral graft. 14 35

Many of the aging Syrian hamsters maintained in our Division spontaneously develop atrial thrombosis accompanied by a consumption coagulopathy. The 50% mortality level is reached earlier by females (16 months) than by males (24 months). The incidence of thrombosis increases with age, beginning at 13.5 months in females and at 21.5 months in males, and the overall incidence (73%) is nearly the same for both sexes. Bilateral ventricular hypertrophy was found in thrombosed hearts. The hearts of most aged hamsters, whether thrombosed or not, had myxoid valvular thickenings and myocardial degeneration. Myodystrophic changes included hypertrophied nuclei, cytoplasmic vacuolation, fiber atrophy, and finally replacement fibrosis. Thrombosis probably resulted from local blood stasis secondary to cardiac failure. These hamsters may be an especially useful model for comparative study of the effects of aging and myocardial degeneration on spontaneous thrombosis.
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PMID:Spontaneous atrial thrombosis in aged Syrian hamsters. I. Incidence and pathology. 14 65

Both deep venous thrombosis and DIC are intermediate mechanisms of disease--both are a consequence of the deposition of fibrin-rich material in blood vessels some distance from the primary site of tissue destruction. The great difference in the sites of fibrin deposition may depend on the extent and site of activation of the clotting mechanism. DIC likely occurs in the fluid phase of the blood as a consequence of massive fibrin formation while thrombosis results from limited fibrin formation at the interface between blood and vessel wall. Leukocytes may be essential for attaching thrombi to the vessel wall in many places.
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PMID:The intravascular generation of fibrinogen derivatives and the blood vessel wall in venous thrombosis and disseminated intravascular coagulation. 14 74

Fibrinogen was depleted in dogs injected with a single dose of bothropase even if pretreatment followed by a continuous infusion of antifibrinolytic drugs was performed during defibrination. The activation of the fibrinolytic system as a secondary effect of the defibrination syndrome induced by bothropase injection was blocked completely by aprotinin (Trasylol) but not by EACA. Plasmin activity in spite of the inhibition of plasminogen activator suggests that, either an excess of activator is released in circulation or a plasmin-antiplasmin complex is dissociated by the circulating fibrin, according to the hypothesis of Ambrus and Markus [1], and Back et al. [4] for the mechanism of fibrinolysis in vivo. An experimental model is suggested for the study of the fibrinolytic mechanism in vivo, by the association of defibrinating agents, antivenom and antifibrinolytic drugs.
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PMID:Experimental defibrination and bothropase: a study on the fibrinolytic mechanism in vivo. 14 12

In states of plasmic hypercoagulability and consumption coagulopathy ethanol favours the non-enzymatic polymerization of circulating soluble fibrinogen fibrin monomer complexes (FFMC) in vitro. The ethanol-gelation test of Godal and Abildgaard makes use of this phenomenon, called paracoagulation. The present studies show that it is also possible to visualize soluble FFMC by means of ethanol-gelation. In the electron microscope, FFMC, polymerized non-enzymatically by ethanol in the spleen, are characterized by plump or slender mycelioid fibrillar precipitates that show a uniform rhythmic transverse striation, a period-coincidental filamentary arrangement and an average periodicity of 23 nm. The ultrastructure demonstrates these ethanol-induced filaments to be in vitro-polymerized fibrin monomer derivatives. Paracoagulation with ethanol allows the identification of soluble FFMC in the tissue prior to the formation of highly polymerized fibrin-rich microthrombi, the established equivalents of the DIC-syndrome. The electron microscope studies also show the existence of a second type of fibrillary structure in the tissue polymerized by ethanol. This second type lacks the characteristic periodicity of fibrin and the period-coincidental arrangement of the filamentary structures, but is characterized by closely packed or chain-like aligned, irregularly sized spherical bodies. There is some evidence that these spherical bodies in vitro represent non-enzymatically polymerized complexes of fibrin monomers and fibrin degradation products (FDP), the equivalent of a limited local or generalized fibrinolysis in vivo.
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PMID:Identification of soluble fibrinogen fibrin monomer complexes by non-enzymatic polymerisation in the tissue. 14 78

A case of liver hemangioma complicated by intravascular coagulopathy is presented because of the rarity of the association. Hemangioma of the liver was suspected by palpation of the liver tumor, scintigraphy and x-ray examination, and confirmed by selective hepatic arteriography in combination with exploratory laparotomy. Intravascular coagulopathy was established by demonstrating secondary fibrinolysis and consumption of platelets and coagulation factors. Unconjugated hyperbilirubinemia due to micro-angiopathic hemolytic anemia was also present. The clinical course of the clotting abnormalities was basically a chronic one with an occasional acute or subacute defibrination process associated with further enlargement of the hepatic tumor. These provide sufficient evidence that the intravascular coagulopathy was closely related with the hemangioma in the liver. Neither ligation of a presumed nutritional artery of the hemangioma nor radiation therapy caused any demonstrable reduction in the tumor size.
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PMID:A case of giant cavernous hemangioma of the liver complicated by intravascular coagulopathy. 14 35

The proteolytic enzymes of the coagulation and fibrinolysis systems as well as others such as kallikrein, activated under pathological conditions can be determined directly, without manipulations of the plasmas, with the synthetic chromogenic substrates. With these substrates it is possible to follow the protease activity in disseminated intravascular coagulation, during thrombolysis and under other conditions. The lack of absolute substrate specificity makes it imposssible to identify the activated proteases.
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PMID:Assay with chromogenic substrates of in vivo activated proteases. 14 48

Two cases of idiopathic adult hemolytic uremic syndrome in which deposits of IgM and C3 were identified in renal arterioles showing fibrinoid necrosis are reported. Fibrin was also identified in the lumina of the involved vessels, but there was no laboratory evidence of disseminated intravascular coagulation. In both cases, serum C3 was decreased and C4 was normal, suggesting involvement of the alternate pathway of complement activation. These two cases suggest that in some instances the adult hemolytic uremic syndrome may be immunologically mediated, and that renal vascular thrombosis is a secondary phenomenon.
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PMID:Adult hemolytic uremic syndrome with renal arteriolar deposition of IgM andC3. 15 58

Changes of prekallikrein in the cases with DIC were investigated, i.e., DIC cases including disseminated metastasis of gastric cancer, acute promyelocytic leukemia and endotoxin shock. Therefore, the trigger substances for this paper were the pathologic cells of the leukemia, the cultured well differentiated adenocarcinoma cells and endotoxin. (1) The lysates of the pathologic cells of the leukemia and the cultured cells showed prekallikrein activation. Endotoxin showed prekallikrein activation via factor XII. (2) Serine proteases (factor Xa, thrombin, plasmin and trypsin) activated prekallikrein in the plasma and the purified prekallikrein. (3) Antithrombin III, aprotinin and FOY inhibited prekallikrein activation. Antithrombin III was promoted by heparin in its inhibitory effect.
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PMID:Changes of prekallikrein in the cases with disseminated intravascular coagulation syndrome. 16 Jan 91


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