Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.6 (thromboplastin)
 13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As a background for the development and testing of phospholipase C in the therapy of post-traumatic and post-surgical intravascular coagulation, highly purified tissue thromboplastin was injected i.v. into rats. The levels of factor V, VII, VIII and blood platelets and the activity of the intrinsic coagulation pathway in general (the cephalin test) were followed. Histological examination of pulmonary, kidney and liver tissue was carried. The dose-response was highly dependent on the injection rate. A marked activation of factor VII and a fall in the activities of factors V and VIII as well as in thrombocyte counts were observed. Very few or no thrombi were seen beyond the pulmonary circulation. The main changes (fibrin-containing thrombi and platelet aggregates) were observed in the lungs during the first 15 min after injection. Atter 15 min virtually no thrombi or platelet aggregates could be detected. The effect of tissue thromboplastin was counteracted by large doses of antithrombin III.
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PMID:The effect of intravenous injection of purified human tissue thromboplastin in rats. 93 13

Serial measurements of coagulation activity, platelet counts, and platelet aggregation were done in patients with full-thickness burns involving 25% or more of body surface area to detect specific changes that might correlate with the onset of septicemia. Mean and maximal values for prothrombin time, partial thromboplastin time, thrombin time, activities of factor V and factor VIII, and concentrations of fibrinogen and fibrinogen-related antigens observed in the presence of bacterial septicemia did not differ significantly from those observed in the absence of septicemia. Mean platelet counts were significantly less with sepsis, but values in individual subjects were not indicative of the presence of septicemia. By contrast, platelet aggregation in response to adenosine diphosphate, epinephrine, and collagen always became severely abnormal with the onset of septicemia but not in the absence of sepsis.
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PMID:Platelet aggregation as a sign of septicemia in thermal injury. A prospective study. 94 30

Polylysine has been demonstrated to dramatically accelerate the rate of the factor Xa catalyzed activation of both prothrombin and prethrombin 1. Under the present experimental conditions (pH 8.0, 23 C), no detectable activation of prothrombin or prethrombin 1 occurs with either factor Xa or polylysine alone. The activation of prethrombin 2, the direct precursor of alpha-thrombin, by factor Xa is not stimulated by polylysine. The activation of either prothrombin or prethrombin 1 by factor Xa in the presence of polylysine is partially inhibited by the presence of 5 mM CaCl2. Electrophoretic analysis in sodium dodecyl sulfate showed that the products that were formed in the above activation system comigrated with the reaction products derived from prothrombin activated by factor Xa in the presence of calcium ions and phospholipid. It is suggested that polylysine stimulates the factor Xa-catalyzes activation of prothrombin by replacing the combination of calcium ions and factor V.
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PMID:Effect of polylysine on the activation of prothrombin. Polylysine substitutes for calcium ions and factor V in the factor Xa catalyzed activation of prothrombin. 98 55

Coagulation and serum F.D.P. studies in 10 leptospirosis patients (5, L. bataviae, 2, L. autumnalis, 2, L. australis, and 1, L. akiyami A.)showed prolongation of prothrombin time, partial thromboplastin time and thrombin clotting time, slight low platelet count, depletion of factor V and slightly high serum F.D.P. in only four cases. Four cases had bleeding and one case died because of severe haemorrhage but with only slight changes in coagulation factors and slightly high serum F.D.P. These findings suggested that the damage of capillary endothelium was more pronounced than the coagulopathy which may be due to liver cell damage.
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PMID:Coagulation studies in leptospirosis. 108 21

The following tests were performed in 15 cases of chronic aggressive hepatitis (CAH), 12 of cirrhosis, and 8 of other forms of chronic disease: liver function, thromboelastogram, prothrombin time (PT), partial thromboplastin time (PTT), determination of factors I, II, V, X and XIII, euglobulin and FDP lysis, and platelet count, shape and agglutinability. At least one haemostasis alteration was observed in nearly every case, the most common being in the thromboelastogram, PTT, prothrombin, and platelet shape and agglutinability. Defects were most marked in cirrhosis and comparison with CAH was significant in the case of PT and factor V. Fibrinolysis was increased in 60% of the CAH group and rarely elsewhere. Haemorrhage was noted in 7 cases of cirrhosis and 1 of CAH. On each occasion, it was more dependent on the serious nature of the disease, rather than defective haemostasis.
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PMID:[Hemostatic changes in the course of different chronic hepatopathies]. 111 9

A simple and rapid one-stage plasma heparin assay based on the heparin-dependent neutralization of activated factor X (Xa) is described. Factor Xa is prepared in a concentration adjusted to produce a clotting time of 18 to 20 seconds when heparin-free plasma is tested in the system. The assay incubation mixture contains "standard human plasma", the heparinized test plasma, cephalin, and factor Xa. Clotting times are measured automatically after incugation and calcium addition. A linear relationship was found between the log of the clotting time and the heparin concentration for the standard curve from which the heparin level is determined. The lower limit of sensitivity is about 0.05 unit heparin per milliliter. Dilution of test plasma is required to bring the heparin level to between 0.05 and 0.2 unit per milliliter. The standard curve is reproducible with a coefficient of variation of 2 to 4 per cent. Ten different, nonheparinized samples had clotting times of 18.9 plus or minus 1.0 (plus or minus 2 S.D.) seconds. Theoretically calculated and experimentally determined heparin levels after pulse injection of heparin agreed well in 5 volunteer subjects with r values between 0.93 and 0.99. This assay is not affected by normal variation in the plasma levels of fibrinogen, prothrombin, and factor V or by the plasma defects induced by coumadin.
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PMID:One-stage assay of heparin. 112 60

Coagulation and fibrinolytic profiles have been studied in two groups of sterility patients receiving low dosage regimens of human gonadotropins for ovarian stimulation. This investigation was prompted by a report of two patients with severe episodes of intravascular coagulation associated with periods of "hyperstimulation" from these drugs. No statistically significant changes were found as a result of administration of one ampoule of human menopausal (HMG) or pituitary gonadotropins (HPG) for 8 days followed by 9000 units of human chorionic gonadotrophin (HCG). A course of 2-3 ampoules HMG on alternate days for longer periods of time prior to administration of HCG also failed to produce significant alterations of the coagulation or fibrinolytic mechanisms. In two patients with severe hyperstimulation there were elevated levels of factor V, platelets, fibrinogen, profibrinolysin, and fibrinolytic inhibitors. Generation of thromboplastin was also increased when plasma was diluted one to fifty in the thromboplastin generation test. These results suggest a possibly increased coagulation potential in patients with "hyperstimulation syndrome" but not in those receiving the low dosage regimens of human gonadotropins more commonly used for ovarian stimulation at the present time.
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PMID:Studies of the coagulation and fibrinolytic systems in hyperstimulation syndrome after administration of human gonadotropins. 114 49

When intermediate-strength thromboplastin was continuously infused into dogs for 10 days or more, platelet counts decreased sharply and factor VIII concentrations decreased by more than 50%. There was little change in plasma fibrinogen, prothrombin, factor V, antithrombin III, plasminogen, prothrombin time, and thrombin time values. When heparin was infused (25-50 U/kg per h) along with the same thromboplastin, there was no change in onset or degree of thrombocytopenia. However, the decrease in factor VIII was abolished and there were significant increases in fibrinogen, prothrombin, and factor V. The absolute concentrations of the various clotting factors seemed to give no indication of their turnover rates. Unexplained is the remarkable heparin tolerance that developed in these dogs.
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PMID:Effect of heparin on chronically induced intravascular coagulation in dogs. 116 71

It is known that the activation of prothrombin to thrombin can proceed via two pathways: one initiated by the prothrombin-converting complex (factor Xa, factor V, phospholipid, and CA2+ ions) and the other initiated by the product, thrombin. A kinetic study has shown that the pathways do not proceed with equal ease under all conditions. At high levels of the converting complex, both go to completion: some prothrombin is always cleaved by thrombin, but the resulting intermediate is then activated to give quantitative conversion to thrombin. At slower rates of activation, the product-initiated pathway occurs to a relatively greater extent. Moreover, the intermediate then is not cleaved further but accumulates, so that the generation of thrombin is curtailed. The reason the intermediate is productive only at higher levels of activator may be partly that it is a poorer substrate for the converting complex than prothrombin. More importantly, the activity of the complex is also modulated by thrombin, which rapidly destroys the activity of factor V and factor Xa in a feedback reaction. These concerted controls ensure that prothrombin activation damps itself. Thus thrombin production occurs as a burst, the size of which is regulated by the amounts of factor Xa and factor V initially available.
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PMID:The control of prothrombin conversion. Kinetic control by mechanisms inherent in two activation pathways. 117 Aug 83

Purified coagulation factors and specific antibodies to factor V and factor X were used to investigate the action of thrombin on factor V and the mechanism by which thrombin-treated factor V influences prothrombin activation. The formation of a complex or complexes between phospholipid, factor V, factor Xa and calcium was demonstrated by column chromatography on Sephadex gel, and by immunological analysis of the column fractions including the use of solid-phase antibodies. Kinetic experiments demonstrated that generation of thrombin from purified prothrombin was accomplished by this complex. Pre-treatment of factor V with trace quantities of thrombin resulted in increased yield and rate of thrombin generation. It was shown that phospholipid became saturated when incubated with increasing concentrations of factor V and that the initial saturating concentration of the latter was reduced by pre-treatment with thrombin. The findings confirm that optimum conversion of prothrombin to thrombin is accomplished by a complex or complexes of phospholipid, factor V, factor Xa and calcium and it is suggested that thrombin plays an autocatalytic role in these reactions.
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PMID:Factor-V activation by thrombin and its role in prothrombin conversion. 119 55


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