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)

Minimal dose heparinization inhibiting clotting factor IXa, Xa, XIa, as monitored by the activated partial thromboplastin time, was compared with conventional intermittent, continuous and regional heparinization during hemodialysis treatment. Blood loss in coil dialyzers was the same. Heparin dosage was reduced markedly. Protamine sulfate and infusion equipment were not required. No bleeding problems were encountered in high-risk patients.
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PMID:Minimal intermittent heparinization during hemodialysis. 47 Nov 42

A comparison has been made of some effects of a semi-synthetic heparin analogue, A73025, and heparin upon platelet function. In several of the in vitro tests performed, such as their potentiating effects on ADP and adrenaline induced aggregation and their effects on the aggregation of washed platelets by activated factor X, heparin proved to be more potent than A73025. Following intravenous injection of twice the quantity of A73025, an equivalent anti-factor Xa activity was obtained, in the agreement with our previous studies. However, it was found that PRP containing heparin and A73025 with comparable anti-Factor Xa acitvity responded differently to the addition of thrombin, as A73025 barely inhibited thrombin induced aggregation. Similarly, A73025 had little effect on the dilute thrombin clotting time of plasma, following intravenous injection. Heparin and A73025 were neutralized to approximately the same degree by a crude PF4 preparation.
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PMID:Comparison of heparin and a semi-synthetic heparin analogue, A73025. II. Some effects on platelet function. 60 58

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

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

The relationship between the antithrombotic and anticoagulant effects of heparin was assessed using venous thrombi in rabbits. Accretion of 125I-fibrinogen onto jugular vein thrombi was used to assess the antithrombotic effect of heparin, and the protamine sulfate titration test (heparin activity) and the activated partial thromboplastin time (APTT) were used to measure its anticoagulant effect. The effect of heparin on jugular vein bleeding times was also measured in a separate group of animals. Fibrinogen accretion was significantly lower with continuous infusion than with intermittent injection. Heparin, given by continuous infusion, produced marked inhibition of fibrinogen accretion (to less than 10% of control accretion) at an APTT value of between 75 and 80 sec (control 34 sec) and at a level of heparin activity of 0.4-0.5 U/ml. Infusion of cryoprecipitate reduced the effect of heparin on the APTT relative to its effect on heparin activity. In these cryoprecipitate-treated animals, marked inhibition of fibrinogen accretion occurred at a similar level of heparin activity (0.4-0.6 U/ml) but at a significantly lower APTT (35-50 sec) than in normal animals. On the other hand, there was a progressive increase in jugular vein bleeding time with both increasing APTT values and heparin levels in both groups of animals.
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PMID:Relationship between the anticoagulant and antithrombotic effects of heparin in experimental venous thrombosis. 83 72

The activated partial thromboplastin time (APTT) has been advocated for monitoring heparin effect. This study was designed to determine the in vitro sensitivity to heparin of commercially available APTT reagents. Heparin was added in increasing concentrations to pooled citrated plasma. Fibrometer APTT determinations were performed at each concentration using General Diagnostics, Ortho, Dade, Hyland, and BBL reagents. A tilt-tube kaolin-activated partial thromboplastin time was also tested using a Sigma partial thromboplastin prepared by the method of Bell and Alton. The General Diagnostics, Sigma, and Ortho reagents displayed linear heparin sensitivity; the General Diagnostics APTT was prolonged 1 1/2-2 1/2 times in a plasma heparin range that prolonged a modified in-vitro Lee-White clotting times 2-3 times. The other reagents were either insensitive, too sensitive, or nonlinear in heparin response. Thus, commercial reagents vary widely in their in-vitro sensitivity to heparin.
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PMID:Variation among commercial activated partial thromboplastin time reagents in response to heparin. 85 45

Heparin activity was assessed in 11 patients who underwent extracorporeal circulation for open-heart surgery. The activated partial thromboplastin time (A-PTT), thrombin time, protamine sulphate titration and factor Xa inhibition assay were used. The patients received heparin 3 mg/kg body weight, and 20 mg/450 ml blood was added to the pump. When the operative procedure was extended beyond 100 minutes patients received an additional 1,5 mg heparin/kg body weight. Protamine sulphate in a dose of 1,5 mg/1 mg heparin, was given to neutralize the heparin activity. The A-PTT was the easiest test which gave reliable results. The factor Xa inhibition assay measured heparin levels most precisely and mirrored the A-PTT results in all but one instance. These results indicate that the protocol employed produced adequate anticoagulation for the bypass procedure in all the patients. Protamine sulphate failed to neutralize heparin adequately after bypass in the 3 patients who received additional heparin during the surgical procedure. The monitoring of heparin activity during and after extracorporeal circulation is a desirable addition to open-heart surgical treatment.
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PMID:The monitoring of heparin activity during extracorporeal circulation. 88 33

Heparin assays based on four different tests of clotting function have been compared with a heparin assay utilizing the potentiating effect of heparin on anti-factor Xa in a group of patients receiving subcutaneous heparin therapy during late pregnancy. It is considered that the anti-factor Xa method is a better indication of the antithrombotic effect of heparin. In the presence of high levels of clotting factors, heparin assays based on tests of clotting function can be misleading.
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PMID:Measurement of heparin in patients receiving subcutaneous heparin therapy. 120 Dec 5

For the therapist, there is only one heparin, characterized by its anticoagulant action, but two methods of administration : intravenous and subcutaneous. Heparin is a true anticoagulant, and directly opposes fibrin formation (antithrombotic action) and potentiates the inactivation of prothrombinase ; this global action, immediately effective, makes heparin undoubtedly superior to the antivitamins K. Nevertheless, its action on thrombogenesis is incomplete : it reacts only slightly or not at all on platelet aggregation and fibrinolysis. In the treatment of phebitis, its efficacity is closely bound with its rational use : early use, continuous and sufficiently prolonged infusion, and carefully adapted dosage are the key factors. The practice of interrupted intravenous injections should be abandoned because it is illogical and dangerous. The subcutaneous method ensures a heparinotherapy in all ways closely comparable with the ideal perfusion. Accidents during heparin therapy are neither more frequent nor more serious than those of a really efficient treatment with antivitamins K. At present, heparin is our most effective weapon in the prevention of post-surgical phlebitis.
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PMID:[Heparins]. 120 36

Heparin is a parenteral antithrombotic agent with efficacy in the treatment and prevention of venous thromboembolic disease and in preinfarctional angina. Accumulating evidence also suggests that heparin is useful in the prevention of coronary artery reocclusion after thrombolytic therapy for acute myocardial infarction, and in the prevention of left ventricular mural thrombosis after anterior wall myocardial infarction. Heparin appears to offer only marginal benefit in reducing mortality when given in combination with thrombolytic therapy and aspirin for acute myocardial infarction. When used for prevention of venous thromboembolism in moderate risk patients, heparin should be given subcutaneously in a dose of 5000 U every 12 hours for 5 to 7 days or until the patient is ambulatory. In higher risk patients, such as those undergoing total hip replacement, heparin should be given subcutaneously every 12 hours in a dose to prolong the activated partial thromboplastin time (aPTT) by 4 to 5 seconds into the upper normal range. When used to treat active venous thromboembolism or the peri-infarctional state, heparin should be given by intravenous infusion with loading and maintenance doses to consistently prolong the aPTT to between 1.5- and 2.5-fold the control value (mean of laboratory's normal range). If constant intravenous infusion is not possible, the drug should be given subcutaneously every 12 hours to consistently prolong the aPTT between 1.5 and 2.5 times control. This regimen is also recommended in pregnant women with venous thromboembolic disease or mechanical heart valves.
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PMID:Heparin therapy. Regimens and treatment considerations. 128 May 66


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