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

Disorders of blood coagulation were investigated before and during a cytostatic combination therapy with vincristine sulphate and iphosphamide (Asta Z 4942) in 12 patients with malignant tumours or haemoblastoses. Thromboplastin time, partial thromboplastin time, thrombin time, heat-dependent fibrin, clot retraction, and clotting factors II, V, VIII, IX, X, and the platelet count were determined. A change in the plasmatic coagulation system attributable to the combination therapy could not be demonstrated in any patient. The influence of the cytostatic combination on the platelet-dependent haemostasis was small; a decrease in platelet count could be observed in only one patient, in whom an additional causative damage to thrombopoiesis due to the underlying disease could be assumed. Regardless of the cytostatic therapy there were indications of a hypercoagulability in 10 patients. This explains the increased susceptibility of such patients for thromboses or consumption coagulopathy.
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PMID:[Influence of cytostatic combination therapy with vincristine sulphate and iphosphamide on blood coagulation]. 111 66

Infusion of autologous hemolyzed blood in humans has served as a model for various experimental investigations for many years. Numerous studies have shown this model to be unattended by any adverse clinical reactions. In this study evidence of subclinical disseminated intravascular coagulation (DIC) was sought in normal humans infused with autologous hemolyzed blood. Hemoglobinemia was induced in 10 experiments by a single injection of frozen-thawed blood and in 4 experiments by such an injection of hemolysate followed by a 5-h maintenance infusion. Mean peak plasma hemoglobin following single dose injections was 540 mg/100 ml, while levels during continuous infusion averaged 240 mg/100 ml. The induction of hemoglobinemia was asymptomatic. Coagulation studies showed no significant alteration in prothrombin time, partial thromboplastin time, thrombin time, clottable fibrinogen, or WBC. Fibrin degradation products were not found. Platelet counts fell slightly in the 5-min postinfusion sample but returned to preinfusion levels within 30 min, suggesting a temporary sequestration of platelets rather than consumption. The induction of moderate brief experimental hemoglobinemia in normal subjects did not result in the development of demonstrable DIC.
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PMID:Coagulation studies during experimental hemoglobinemia in humans. 112 Jul 40

Disseminated intravascular coagulation was induced in dogs by the infusion of a fibrinolytic inhibitor followed by thrombin. The deposition of microthrombi in the lung was demonstrated by radioactive labelling of platelets and fibrinogen.
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PMID:Thrombin-induced disseminated intravascular coagulation in the dog. I: Demonstration of microthrombi in lung. 114 85

Disseminated intravascular coagulation (DIC) was induced in anaesthetized dogs by the infusion of a fibrinolytic inhibitor followed by thrombin. The occurrence of DIC was confirmed by haematological and histological examinations. After the thrombin infusion there was a progressive reduction in cardiac index and systemic arterial pressure, only four of the 14 dogs surviving for 4 hr. Pulmonary artery pressure increased after the thrombin infusion, but decreased subsequently in seven animals allowed to breathe spontaneously. In these animals, there was an increase in respiratory rate, minute volume and deadspace/tidal volume ratio, but there were no changes in the arterial-to-alveolar PCO2 difference. Arterial PCO2 and PO2 decreased, but there were no significant changes in total venous admixture. In seven dogs submitted to controlled ventilation, arterial PO2 decreased to the same extent, but there were no significant changes in arterial PCO2, deadspace/tidal volume ratio or venous admixture.
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PMID:Thrombin-induced disseminated intravascular coagulation in the dog. II. Cardiorespiratory changes during spontaneous and controlled ventilation. 114 86

Simultaneous platelet and fibrinogen survival with 75Se selenomethionine was determined in eight patients with acute infectious hepatitis of intermediate severity. Fibrinogen survival alone was estimated in another nine patients, seven of whom were receiving heparin treatment. Platelet survival was found to be normal (7-9 days) in seven of the 8 patients; it was reduced 4,6 days) only in one patient, who was also affected by measles. Fibrinogen survival was markedly reduced (1-3.7 days) and fibrinogen turnover sharply increased (0.59-2.80 mg/ml/day) in all but one patient, who had thalassaemia major, with normal fibrinogen survival and fibrinogen turnover. Heparin treatment did not affect either platelet survival or fibrinogen turnover. In all patients the coagulation defect was mild and no sign of disseminated intravascular coagulation or of increased fibrinolytic activity could be demonstrated by routine tests. These results are consistent with the hypothesis that in acute infectious hepatitis the decreased survival and increased turnover of fibrinogen might be due to a pathological pathway of defibrination in dependent of thrombin of plasmin.
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PMID:Platelet and fibrinogen survival with 75Se selenomethionine in acute infectious hepatitis. 115 8

After envenomation by the timber rattlesnake (Crotalus horridus horridus) a young man showed massive swelling and ecchymoses of the involved extremity, generalized petechiae and a large hematoma of the left upper eyelid. Two weeks later he was completely well. The first blood sample was incoagulable and showed high titers of fibrin split products by the MISFI and staphylococcal clumping tests. Immounoelectrophoresis showed both D and E fragments, but only D was present at 18 hours. The profound thrombocytopenia and hypofibrinogenemia gradually improved, and split products disappeared. In vitro the venom had thrombin-like activity, clotting fibrinogen or plasma and aggregating platelets. These activities could be inhibited by antivenom but not by heparin. There was no evidence that thrombin formation was actually involved: hence, the syndrome is called DIC-like.
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PMID:DiC-like syndrome after envenomation by the snake, Crotalus horridus horridus. 116 34

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

Changes in the clotting system, as well as morphological and functional alterations corresponding to that of the pathologic phenomenon of disseminated intravascular coagulation (DIC) or consumption coagulopathy, were produced by thrombin infusion (550 NIH U X kg-1 X h-1) in rats and simultaneous inhibition of fibrinolysis by PAMBA (100 mg/kg). Changes in the fibrinogen level and platelet count as well as the appearances of fibrin monomers and the formation of microthrombi in several organs were evaluated. Simultaneously, the function of the respiratory system was investigated by continuous measurement of oxygen consumption as well as elasticity and water content of the lung. From the time course of the alterations in the several parameters, conclusions can be drawn for the pathogenesis and the possible therapeutic influence on DIC.
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PMID:Studies in experimental animals on disseminated intravascular coagulation (DIC). 119 9

The formation of fibrin clots or circulating soluble fibrin is accompanied by the appearance of fibrinopeptides. Measurement of the fibrinopeptide concentration in plasma can provide important information on the rate of conversion of fibrinogen to fibrin by thrombin. This rate varies under different physiologic and pathologic conditions. Fibrinopeptide A is a better molecular marker of the conversion than fibrinopeptide B since it is the first peptide to be cleaved by thrombin. A radioimmunoassay technique has been developed for the quantitative determination of human fibrinopeptide A. The procedure detects human fibrinopeptide A at a concentration of approximately 0.05 ng/ml. The variation of fibrinopeptide A content in normal persons may reflect its rapid formation and catabolism. A significantly increased concentration of this peptide was found in a patient during defibrination therapy with a purified enzyme from the venom of Agkistrodon rhodostoma and in patients suffering from retinal vascular occlusions.
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PMID:Determination of human fibrinopeptide A by radioimmunoassay in purified systems and in the blood. 120 41

The cardiorespiratory effects of thrombin-induced disseminated intravascular coagulation (DIC) were studied in two groups of dogs. The main changes were a reduction in cardiac output and arterial pressure, an increase in pulmonary artery pressure and, an increase in pulmonary artery pressure and an increase in venous admixture. In one group of dogs the reduction in cardiac output was diminished by the infusion of dextran 35 ml/kg body weight. This resulted in an increased pulmonary artery pressure but no significant differences in the indices of the efficiency of gas exchange. However, the haemodilution resulted in a lower mixed venous and arterial PO2 in this group of dogs.
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PMID:Thrombin-induced disseminated intravascular coagulation. III:Modification by dextran infusion. 121 44


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