Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.6 (thromboplastin)
13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 12 vascular and 17 trauma cases the changes in the coagulation system due to intraoperative autotransfusion (IAT) were examined immediately after the IAT as well as 24, 48, 72 h and one week later. The following parameters were monitored: 1. Platelet count. --2. Prothrombin-time, partial-thromboplastin-time, factors II, V, VII, X and thrombin-clotting-time. --3. Fibrinogen, alpha-1-antitrypsin, alpha-2-macroglobulin, antithrombin III and plasminogen in 5 trauma cases. --4. Euglobulin-Lysis-Time. --After the IAT a loss of platelets, factors I, II, V, X, plasminogen and antithrombin III was found. Alpha-1-antitrypsin and alpha-2-macroglobulin remained unchanged or showed a slight increase. 24 h after treatment with Ugurol and heparin, fresh frozen plasma, fibrinogen and Cohn I-fraction in selected cases, an increasing normalisation of most parameters was seen, except for the plasma proteins active in coagulation. They showed a combination of "consumption coagulophathy" and "hyperfibrinolysis" up to the 7th day. Under treatment outlines above even marked laboratory changes remained without any clinical significance. Thus our results confirm that IAT does not cause any additional irreversible damage to the coagulation system. Therefore IAT can be considered as method of choice for the emergency treatment of massive bleeding.
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PMID:[Intraoperative autotransfusion and its influence on the blood-clotting-system (author's transl)]. 59 9

A pharmacokinetic study of intraperitoneal heparin was undertaken in eleven chronic renal failure patients as a guide for its therapeutic use in peritoneal dialysis. The intraperitoneal heparin was assayed as the activated-partial-thromboplastin time (A-PTT) of peritoneal aspirate or outflow dialyzate added to control plasma. This was noted to decay relatively slowly, the mean t 1/2 of heparin in the peritoneal cavity being 10.8 +/- 0.93 hr. The heparin cofactor antithrombin III determined by both immunological and functional methods was found to be present in low concentration in residual peritoneal fluid aspirated prior to commencing dialysis. Generally this was less than one-third of normal plasma values, and with the repeated dilution and outflow sequences of dialysis the cofactor concentrations rapidly fell to negligible levels that were incapable of activating any heparin present. Systemic blood coagulation was unaffected by single 10000 U doses of heparin administered intraperitoneally in that plasma A-PTT values were not lengthened when measured over the ensuing six hours.
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PMID:Activity of intraperitoneal heparin during peritoneal dialysis. 63 Jul 40

The factor Xa inactivating function of antithrombin III is measured automatically by an amidolytic method, adapted to a centrifugal analyser. Plasma is diluted in buffer with heparin. In stage I, diluted plasma is incubated with excess factor Xa. Heparin accelerates the saturation of antithrombin with factor Xa. In stage II, remaining factor Xa is determined with the chromogenic substrate Bz-Ile-Glu-Gly-Arg-pNA. The precision of the present assay compares favourably with that of the clotting assays and immunoassay. There is a close correlation (r = 0.82) between the results obtained with this assay and the immunoassay of antithrombin III.
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PMID:Automated antithrombin III assay with a centrifugal analyser. 65 85

A simple assay method for platelet factor 4 is described. When factor Xa was added to a system containing antithrombin III in excess and heparin in low concentration, the amount of factor Xa immediately inactivated was found to be a function of the concentration of heparin. When an antiheparin such as platelet factor 4 was added, an increase of the residual activity of factor Xa was observed. The magnitude of this increase was shown to be correlated to the amount of heparin inactivation in the system. Platelet factor 4 could be assayed when the concentrations of antithrombin III, heparin, and factor Xa were maintained at a constant level and in excess. As an indicator of the reaction, factor Xa was measured with the chromogenic substrate benzoyl-Ile-Gou-Gly-Arg-p-nitroanilide (S-2222).
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PMID:A simplified assay method for platelet factor 4 in plasma and in platelets with a chromogenic substrate. 72 Sep 57

There are three categories of antithrombotic agents: drugs which prevent fibrin fromation (the anticoagulants and defibrinating enzymes), drugs which prevent platelet adhesion or aggregation (the antiplatelet drugs), and thrombolytic drugs which induce fibrin degradation. Clinical studies have now led to a better understanding of the relative value of these drugs in different thrombotic disorders. In addition, knowledge of the mechanism of action of some of these drugs has recently been much advanced. The anticoagulant drugs in clinical use are heparin and the oral anticoagulants. Heparin is a potent inhibitor of several steps on the intrinsic coagulation pathway through its effect on a plasma cofactor, antithrombin III. its action is immediate, but heparin must be given parenterally. Oral anticoagulants act more slowly, by reducing the hepatic synthesis of biologically active factors II, VII, IX and X, but can be given by mouth. Heparin is therefore most suitable for starting anticoagulant treatment, while oral anticoagulants are generally used for prolonged therapy. The value of the anticoagulants as antithrombotic agents has been best assessed by studying their effectiveness in preventing and treating venous thromboembolic disease. Oral anticoagulants have been repeatedly shown to prevent venous thrombosis and pulmonary embolism in patients at high risk of developing these complications. However, the increased risk of postoperative bleeding has prevented their widespread use for this purpose in surgical patients. Recently, the use of low doses of heparin, given subcutaneously before and after surgery, has been shown to markedly reduce the incidence of venous thrombosis and pulmonary embolism (including fatal pulmonary embolism) after major elective abdominal surgery, and to produce only a slight increase of postoperative bleeding. This represents a major advance in anticoagulant prophylaxis of venous thromboembolism insurgical patients. However, low dose heparin prophylasix is relatively ineffective in patients having hip surgery, and has not been evaluated in patients having other types of orthopaidic surgery. There is direct evidence that antocoagulant therapy prevents death and recurrent embolism in patients who have developed pulmonary embolism, and considerable indirect evidence that it prevents pulmonary embolism, and considerable indirect evidence that it prevents pulmonary embolism (and death from pulmonary embolism) in patients who have venous thrombosis. The incidence of further venous thromboembolism or bleeding during treatment appears to be minimised when heparin is given by continuous intravenous infusion in a dose sufficient to produce a moderate, but no excessive, prolongation of a heparin-sensitive, in vitro coagulation test. The tests most commonly used to monitor heparin therapy was based on either the whole blood clotting time or the activated partial thromboplastin time...
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PMID:Antithrombotic drugs: part I. 78 43

When activated factor X (Xa) inhibitory activity of serially diluted human and rabbit plasma is determined in a low salt assay, a lineare plot is obtained for human, but not for rabbit plasma. When a high salt assay is used, the dilution curves for both human and rabbit plasma are linear, and qualititive as well as quantitative differences are essentially eliminated. On Sephadex G-200 chromatography Xa inhibitory activity of human and rabbit plasma appears in two peaks. With the low salt assay the first and second peaks for human plasma contain respectively 30%, and 70% of the activity; whereas with rabbit plasma these values are greater than 95% and less than 5% of the activity. With the high salt assay the figures for human plasma are less than 5% and greater than 95%, and with rabbit plasma 65 +/- 3% and 35 +/- 3%, respectively. With the high salt system, rabbit plasma shows a continuous increase in Xa inhibitory activity with increasing heparin concentrations, similar to that obtained with human plasma. In the high salt system the relative contributions of antithrombin III to Xa neutralization in human and rabbit plasma are different. However, in experiments in which Xa inhibitory activity of antithrombin III is altered by heparin, a simple formula, Total activity (%) = 65% + 0.35 x human plasma (%), permits translation of rabbit data on the Xa-antithrombin III-heparin reaction to man. On the basis of these findings, the rabbit model can effectively be used to study the Xa-antithrombin III reaction.
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PMID:The rabbit as an animal model for the activated factor X-antithrombin III-heparin reaction. 87 92

Factor VIII is present in plasma in a precursor or inactive form. When bovine factor VIII that has been purified approximately 10,000-fold is incubated with thrombin, an activated product is formed which participates in the conversion of factor X to factor Xa in the presence of factor IXa, calcium ions, and phospholipid. This activated product, which has been tentatively identified as activated factor XIII, was stable when formed in the presence of 0.25M CaCl2 but was rapidly inactivated in the absence of CaCl2. It was inhibited by diisopropyl phosphorofluoridate and antithrombin III, suggesting that it is a serine enzyme. The exact role of this serine enzyme in the intrinsic pathway of coagulation remains to be established.
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PMID:Formation of a serine enzyme in the presence of bovine factor VIII (antihemophilic factor) and thrombin. 87 60

Possible increased activation of the coagulation pathway was measured in a group of patients with neoplastic diseases. In addition to standard tests, the thromboplastin generation test, thrombin generation test and immunologic and coagulant activities of both Factor VIII and antithrombin III were utilized in the evaluation. The correlation between immuno-Factor VIII (VIII-Ag) and its clotting activity (VIII-C1) was good (r = 0.83). In contrast, this was not the situation for antithrombin III-Ag and its clotting activity. Thromboplastin generation was accelerated in 60% and thrombin generation was accelerated in 40% of the patients. Fibrinogen was elevated in half the cases: in most of these patients, thrombin times were slightly prolonged. These results indicate that some patients who have cancer have abnormal clotting patterns and are often in a potentially hypercoagulable state that is reflected by the thromboplastin generation test, thrombin generation test, and high levels of Factor VIII (both VIII-Ag and VIII-C1).
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PMID:Antithrombin III and Factor VIII in patients with neoplasms. 87

The coagulation and fibrinolytic systems were investigated in a group of patients with essential hypertension during pregnancy, and the findings were compared with those of normal gravid women. Patients with essential hypertension exhibited the following significant differences: shortened partial thromboplastin times, thrombocytopenia, and decreased antithrombin III levels. Euglobulin lysis times and assays for fibrin breakdown products suggest that essential hypertension is not associated with changes in the fibrinolytic mechanism. Until more sophisticated studies can be performed on such patients, it cannot be concluded that the increased coagulability observed in pregnant patients with essential hypertension represents a state of intravascular coagulation.
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PMID:Coagulation and the hypertensive diseases of pregnancy. 91 Aug 18

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


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