Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In thrombin-induced DIC, acetylsalicylic acid (ASA) prevents the strong initial fall in platelet count and the obturation of the microvasculature of the lung with platelet aggregates. During the DIC reaction increasing inhibition of aggregability of circulating platelets against collagen and ADP is observed. Furthermore, ASA prevents the increase in the plasma haemoglobin level caused by DIC.
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PMID:[Effect of ASS on platelet function in experimental DIC]. 9 74

Liver changes and associated host responses were evaluated in four groups of male rats, weighing 300 +/- 20 gm., which received intravenous injection of 2.2 times 10(9) live Escherichia coli. This bolus was given either without additional treatment (group A) or prior to the following regimens: intramuscular injection of gentamicin sulfate, 5 mg. per kg. (group B); intravenous injection of methylprednisolone sodium succinate, 40 mg. per kg. (group C); and intramuscular injection of gentamicin immediately after methylprednisolone sodium succinate treatment (group D). Rats given injections of saline or methylprednisolone sodium succinate served as controls. Survival rates at 10 and 20 hours were 25 per cent and 4 per cent for group A; 44 per cent and 28 per cent for group B; 94 per cent and 70 per cent for group C; 98 per cent and 98 per cent for group D, respectively. In rats of groups A and B, killed at 1, 2, 4, and 6 hours, progressive liver changes included intravascular sequestration of rapidly degranulating leukocytes, fibrinous deposits, and platelet aggregates in sinusoids as well as in spaces of Disse adjacent to subendothelial collagen, and extensive Kupffer cell disruption in association with severe midzonal necrosis. These alterations were accompanied by progressive hypoglycemia and elevations of serum enzymes, glutamic pyruvic transaminase, lactate dehydrogenase, and glutamic oxaloacetic transaminase. Hematologic studies revealed that E. coli bacteremia results in rapid leukopenia and disseminated intravascular coagulation primarily due to activation of the intrinsic coagulation pathway. All above reactions were delayed and markedly reduced in rats treated with methylprednisolone sodium succinate. The results indicate that antibiotic treatment of lethal, Gram-negative bacteremia is effective only in conjunction with early steroid treatment. The protective effects of glucocorticoids on the liver microcirculation and polymorphonuclear leukocytes appear to play a basic role in preventing the early development of disseminated intravascular coagulation, hepatocellular necrosis, and associated major host responses, thereby attenuating lethality of gram-negative septic shock.
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PMID:Glucocorticoid and antibiotic effects on hepatic microcirculation and associated host responses in lethal gram-negative bacteremia. 36 36

A patient with clinical and laboratory evidence of disseminated intravascular coagulation associated with deep-vein thrombosis and pulmonary embolism developed a qualitative platelet abnormality characterized by a defective release reaction. Second-phase aggregation induced by ADP and adrenaline was impaired, and reduced collagen-induced aggregation was accompanied by defective release of ADP and ATP. The decrease in total platelet ATP and ADP, the high ATP:ADP ratio in the presence of normal amounts of metabolic adenine nucleotides, and the low content of serotonin associated with abnormal uptake and metabolism of the exogenous amine suggested that the defective platelet function was due to lack of the platelet organelles in which serotonin and nonmetabolic adenine nucleotides are normally stored. Acquired storage pool disease is likely to be related to exposure of circulating platelets to aggregating agents, with their degranulation occurring during disseminated intravascular coagulation.
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PMID:Acquired storage pool disease in platelets during disseminated intravascular coagulation. 96 91

The therapeutic efficiency of two glucocorticoids (hydrocortisone and dexamethasone) on endotoxin-induced intravascular coagulation was investigated in the rat. Coagulation and platelet aggregation studies were performed and plaminogen was assayed. Our results indicate that pretreatment of the animals with large doses of these steroids within a few hours prior to endotoxin totally prevents the consumption in Hageman factor, measurable contact product activity, platelets, fibrinogen, plasminogen, and the loss in platelet aggregability and serotonin. In addition to this, the hypercoagulable state consecutive to endotoxin, characterized here by shortenings in the partial thromboplastin and recalcification times and by an increase in the availability of platelet procoagulant activity, was also totally prevented by the steroid pretreatment. On the other hand, it is shown that these glucocorticoids do not interfere in the normal rat with platelet aggregation (tested with thrombin,adenosine diphosphate, and collagen), but with the availability of platelet procoagulant activity. This last phenomenon, in addition to that of an interference in vivo with the mechanism of activation of Hageman factor, are believed to be responsible for prevention by glucocorticoids of endotoxin-induced disseminated intravascular coagulation.
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PMID:Prevention by glucocorticoids of disseminated intravascular coagulation induced by endotoxin: mechanisms. 109 78

The role of platelet aggregation and coagulo-fibrinolytic systems in thrombogenesis of lactic acid-induced pulmonary thrombosis in rat were studied using an anti-coagulant, platelet aggregation inhibitor, fibrinolytic or anti-fibrinolytic agents. In normal rat, heparin (2.5 mg/kg), acetylsalicylic acid (30 mg/kg) and tranexamic acid (100 mg/kg) suppressed specifically coagulation, platelet aggregation induced by collagen or thrombin and fibrinolysis respectively. Urokinase (10,000 units/kg) activated powerfully fibrinolytic system in addition to suppressing slightly platelet aggregation. The pretreatment with heparin, acetylsalicylic acid or urokinase markedly prevented the formation of thrombus initiated by the infusion of lactic acid at the doses used. Additive effect was also obtained by combined administration of these agents. On the other hand, it was interesting to note that tranexamic acid (100 mg/kg) did not affect the thrombus formation at all despite a potent anti-fibrinolytic effect of this agent. These results indicate that both platelet aggregation and enhancement of coagulation activity are important factors responsible for the formation of thrombi in DIC, while the fibrinolytic activity in blood seems not to be involved in it. On the basis of the findings, mechanism for triggering activation of coagulation and platelet aggregation is also discussed here.
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PMID:Patho-physiological studies on lactic acid-induced pulmonary thrombosis in rat. I. Effect of heparin, acetylsalicylic acid, urokinase and tranexamic acid. 118 8

Increased blood loss is a major contributory factor to postoperative short- and longterm outcome in orthotopic liver transplantation (OLT). Hyperfibrinolysis, occurring mainly in the anhepatic phase, and disseminated intravascular coagulation (DIC), starting immediately after reperfusion, have been observed to parallel increased bleeding tendency. However, other factors may also contribute. For the first time we investigated platelet aggregation during the course of 10 OLTs and found a marked reduction of adenosine diphosphate-, collagen-, and ristocetin-induced platelet aggregation immediately after reperfusion. Since this is the point at which increased bleeding tendency is known to occur, it would seem that, apart from DIC and hyperfibrinolysis, an intermediate dysfunction of platelet aggregation may be a major cause of intraoperative bleeding.
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PMID:Decreased platelet aggregation after reperfusion in orthotopic liver transplantation. 154 50

The development of disseminated intravascular coagulation (DIC) during a controlled IV infusion of concentrated ascitic fluid was studied in a group of patients with cirrhosis and refractory ascites. Nine studies were performed on patients who had not received prophylactic antiplatelet therapy. All developed laboratory evidence of DIC. The total collagen infused, estimated by ascitic hydroxyproline concentration, correlated significantly with both the prolongation of the partial thromboplastin time with kaolin (r = 0.8628; P less than 0.005) and the decrease in platelet count (r = 0.5674; P less than 0.05). The changes in the coagulation profile were reversible on ceasing the infusion, returning to baseline levels within 12 hours. There were no changes in the coagulation profiles of four patients studied 48 hours after beginning antiplatelet therapy with aspirin and dipyridamole. It is concluded that the infusion of concentrated ascitic fluid into a peripheral vein of patients with cirrhosis results in DIC, the severity of which correlates with the amount of collagen infused and which is completely prevented by inhibiting collagen-induced platelet aggregation. The results support the hypothesis that the DIC that complicates ascites infusion into the systemic circulation is largely related to ascitic fluid collagen.
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PMID:Coagulopathy during ascites reinfusion: prevention by antiplatelet therapy. 155 39

Five antiplatelet agents have been isolated from Chinese herbs. Apigenin and magnolol are inhibitors of thromboxane synthesis, while osthole, protopine and norathyriol are inhibitiors of phosphoinositide breakdown. Thirty min after intraperitoneal (i.p.) administration of these drugs, tail bleeding time of mice was prolonged markedly in a dose-dependent manner by norathyriol, protopine, osthole and magnolol, but not by apigenin. However, the antiplatelet agents (up to 200 mg kg-1, i.p.) could not prevent acute thromboembolic death in mice. In endotoxin-induced experimental disseminated intravascular coagulation in rats, norathyriol (50-100 mg kg-1, i.p.) prevented the decrease in platelet counts and fibrinogen, and the prolongation of plasma prothrombin time. Norathyriol (100 mg kg-1, i.p.) also suppressed ex-vivo platelet aggregation induced by collagen and ADP in rat plasma.
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PMID:Antihaemostatic and antithrombotic effect of some antiplatelet agents isolated from Chinese herbs. 168 29

Exposure of subendothelial collagen and release of tissue thromboplastin render possible activation of both the internal and external coagulation cascades in traumatic lesions of the brain. Disseminated intravascular coagulation (DIC) is well described in brain lesions and may contribute to the haemorrhagic tendency in brain-injured patients. DIC is also suggested as a contributory factor for the degree of secondary brain damage and the development of pulmonary complications and tardive intracranial haematomata. The literature concerning DIC and traumatic brain damage is, however, difficult to assess as many of the materials include multitraumatized patients and the diagnostic criteria for DIC vary. In addition, it is difficult to differentiate between normal physiological phenomena and genuine pathological processes. No controlled and randomized investigations concerning the effects of specific antithrombotic treatment of DIC in traumatic lesions of the brain are available. It is recommended that patients with brain injuries should be examined for the development of disturbances of coagulation and that the relevant laboratory investigations should be included in assessment of this patient group.
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PMID:[Coagulation disorders in traumatic brain injuries]. 186 29

This is a very rare case report of Goodpasture's syndrome with IgA antibasement membrane antibody. A 43-year old male was admitted because of severe dyspnea with slight hemoptysis. Chest X-ray demonstrated extensive bilateral infiltrates with air bronchogram, predominantly in the right lung. Laboratory data on admission showed severe anemia and moderate renal impairment. The pulmonary infiltrates resolved spontaneously within 10 days. Goodpasture's syndrome or collagen vascular disease was suspected and he underwent a percutaneous renal and transbronchial lung biopsy. The renal biopsy showed crescent formation affecting 70-80% of glomeruli. Linear IgA deposits, but not IgG, were demonstrated along the glomerular basement membrane by the direct immunofluorescence procedure. The lung biopsy contained many hemosiderin-laden macrophages in the lumen of the alveoli and showed mild thickening of alveolar walls. However, linear immunoglobulin deposits on the alveolar capillary basement membrane were not demonstrated by direct immunofluorescence. The diagnosis of Goodpasture's syndrome with IgA antibasement membrane antibody was made. His serum was negative for antibasement antibody by indirect immunofluorescence. He was treated with prednisone, 30 mg daily. His pulmonary symptoms and anemia improved markedly, but his renal function did not change. Thirteen months after his first admission, he suffered from severe bacterial pneumonia, which was complicated by disseminated intravascular coagulation. He died of respiratory failure. Autopsy was rejected.
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PMID:[A case of Goodpasture's syndrome with IgA antibasement membrane antibody]. 221 6


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