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)

Antithrombin III is one of the main inhibitors in the blood coagulation mechanisms. Thrombin and factor Xa are slowly inactivated by it, as well as other serine proteinases of the coagulation mechanisms. Heparin tremendously accelerates the inhibitory function of antithrombin III. In the process antithrombin III activity is also reduced. Heparin retards the thrombin-fibrinogen reaction, but otherwise the effectiveness of heparin as an anticoagulant depends on antithrombin III in laboratory experiments, as well as in therapeutics. The activation of prothrombin is inhibited, and any thrombin or other vulnerable protease that might generate becomes inactivated. The measurement of antithrombin III concentration in blood is now achieved by research methods, as well as by methods that are practical for routine use. The tests require either thrombin or factor Xa as substrate, and could be specific for antithrombin III. There are congenital as well as acquired deficiencies of antithrombin III. The inhibitor is also found in tissues.
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PMID:Antithrombin III. Theory and clinical applications. H. P. Smith Memorial Lecture. 34 19

Thrombin or factor Xa added to plasma are inactivated by antithrombin III (At-III). The inactivation is accelerated by heparin, permitting assay systems which rapidly measure the At-III content of diluted plasma. Without heparin, the slow inactivation rates may be measured. Existing activity assays (fibrinogen or chromogenic substrates) and immunoassays of At-III have been reviewed. Correlation studies show a close correlation between the results of immunoassay and the results of most activity assays. In health, a narrow range of At-III has been found. The level is low in infancy. Fertile women have on the average somewhat lower levels than men. In old age, the level tends to drop. In clinical material studied with amidolytic assays, subnormal At-III levels were found in hereditary deficiency, liver disease, disseminated intravascular coagulation and in some cases with acute thrombosis. The amidolytic assays are rapid to perform, do not require experience in clotting technique and seem preferable in clinical routine work.
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PMID:Antithrombin III: critical review of assay methods. Significance of variations in health and disease. 35 Jul 29

The development of synthetic inhibitors of thrombin and of related arginine-specific esteroproteases is reviewed. The superiority of bis- and tris-benzamidines over benzamidine is disccussed and related to the presence on the enzyme of secondary binding sites beyond the specificity pocket. It is demonstrated that inhibitors with marked specificity for a single enzyme can be produced, and with the help of such selective compounds it is shown that inhibition of factor Xa is more significant for overall anticoagulant effect than inhibition of thrombin.
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PMID:Current concepts on action of synthetic thrombin inhibitors. 35 Jul 30

During normal pregnancy, the concentrations of many of the clotting factors rise, thereby increasing the potential to generate fibrin. There is also evidence of increased thrombin activity during normal pregnancy which sharply increases during placental separation. Antithrombin III, the main inhibitor of thrombin and activated factor X, shows no compensatory rise during pregnancy but increases during the puerperium. Plasminogen and antiplasmin concentrations rise during pregnancy but systemic fibrinolytic activity, as measured by the euglobulin lysis time, is markedly depressed during pregnancy; the reduced fibrinolytic activity returns to non-pregnant values very soon after delivery. The loss of fibrinolytic activity is presumed to be loss of plasminogen activator, because when this is added in excess in the urokinase sensitivity test, the fibrinolytic response is normal. The capacity for localized fibrinolytic activity is not lost, however, because fibrinolytic degradation products are slightly raised during pregnancy. The overall pattern is one of increased coagulant and reduced fibrinolytic capacity during pregnancy which may protect the pregnant woman against the haemostatic challenge of placental separation.
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PMID:Blood clotting and fibrinolysis in pregnancy. 38 69

We have tested a platelet aggregation inhibitor in the incubation fluid of deendothelialized fragments of the rat aorta and compared it with that of "intact" fragments. Some of the properties of the aortic inhibitor, and its effects on platelet adhesion to collagen fibrils, on platelet factor-3 (PF-3) availability, and on the activated partial thromboplastin time (APTT) and thrombin time (TT) were also evaluated in comparison with similar effects exerted by PGI2. We found that the incubation fluid of deendothelialized aortic samples contained inhibitor activity comparable with that of "intact" samples. The aortic inhibitor had similar properties to PGI2. The aortic inhibitor and PGI2 slightly inhibited light transmission changes of EDTA-PRP following exposure to collagen. However, scanning electron microscopy showed no appreciable difference in platelet adhesion to collagen fibrils. PGI2 and the aortic inhibitor inhibited Kaolin-induced PF-3 availability, but did not prolong the APTT or TT.
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PMID:Generation of a PGI2-like activity by deendothelialized rat aorta. 38 19

The vessel wall contains powerful inhibitors of thrombogenesis. One substance, a proteoglycan, is a strong anticoagulant but has only a limited effect on platelet aggregation. It prolongs the thrombin clotting time and partial thromboplastin time, but only blocks platelet aggregation induced by thrombin. Another vessel wall constituent, a prostaglandin derivative (prostacyclin), is a potent inhibitor of platelet aggregation. It antagonizes platelet aggregation induced by a variety of agents including adenosine diphosphate, collagen, arachidonic acid and thrombin; however, its only effect on coagulation is through the inhibition of platelet factor-3 release. Proteoglycans and prostacyclin comlement each other's antithrombotic activities, and together serve to limit the hemostatic response of blood to vessel wall injury. Vessels devoid of the intima continue to produce prostacyclin. Prostacyclin produced by these vessels is probably more important than that produced by vessels with the intima in the prevention of thrombus deposition.
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PMID:Vascular substances that modulate blood-to-vessel interactions. 39 10

A 10-year-old boy had a severe lifelong hemorrhagic disorder that had necessitated more than 50 hospitalizations. Laboratory examination showed prolonged bleeding, clotting, partial thromboplastin, prothrombin, and thrombin times. These findings were due to a potent inhibitor of the thrombin-fibrinogen reaction. This inhibitor was similar to heparin in that it acted immediately and did not interfere with the coagulant activities of certain venoms. It differed from heparin in not being adsorbed to barium citrate or neutralized by protamine sulfate. The inhibitory effect was found in the alpha1-globulin fraction. It was identified immunologically and functionally as a double-banded alpha1-antitrypsin of a previously unreported phenotype. The inhibitory effects were depressed by trypsin and heterologous anti-alpha1-antitrypsin.
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PMID:Antithrombin Pittsburgh: an alpha1-antitrypsin variant causing hemorrhagic disease. 41 31

A prospective study of hemostatic abnormalities in 108 cancer patients was undertken at an oncology clinic in a university teaching hospital. Tests included Quick prothrombin time, activated partial thromboplastin time, thrombin time, platelet count, modified Ivy bleeding time, fibrinogen, fibrin degradation products (FDP), euglobulin lysis time, protamine sulfate test, and factor V, VII, VIII and X assays. Ninety-eight per cent of the patients had one or more abnormal coagulation tests. The commonest abnormalities were elevated fibrin degradation products and prolonged thrombin time. Thrombocytosis occurred in 57% of patients, hyperfibrinogenemia in 46%, thrombocytopenia in 11%, and non had hypofibrinogenmia. It is suggested that platelet count, fibrinogen concentration, and serum FDP assay are the most useful tests in assessing the hemostatic abnormalities in cancer patients, although thrombin time, factor V assay, and bleeding time may also be helpful. The peripheral blood smears of 53 patients were reviewed, and only one showed microangiopathic hemolytic anemia. The data illustrate that subclinical coagulopathy is relatively frequent in patients with malignancy.
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PMID:Hemostatic abnormalities in malignancy, a prospective study of one hundred eight patients. Part I. Coagulation studies. 42 Jan 61

A study of coagulation has been performed on 8 chronic renal failure patients receiving carbenicillin therapy. All showed a prolongation of the bleeding, recalcification, partially-activated thromboplastin, prothrombin and thrombin times. These findings suggest the presence of an anticoagulant with an heparin-like mode of action. In vitro tests suggest that carbenicillin may be this factor. We have also shown that the drug produces a disturbance in the normal polymerization process. The implications of these findings for the treatment of (CRF) patients with carbenicillin are discussed.
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PMID:Effects of carbenicillin on blood coagulation: a study in patients with chronic renal failure. 42 53

The effects of three widely spaced levels of bacterial contamination of reagent water on several chemistry, radioimmunoassay, and coagulation procedures were studied. These included determinations of lactate dehydrogenase, creatine kinase, aspartate transaminase, alkaline phosphatase, blood urea nitrogen, total protein, thyroid-stimulating hormone, digoxin, thrombin time, activated partial thromboplastin time, and prothrombin time. Statistical analyses included calculations of means and coefficients of variation, and analysis of variance, as well as correlation coefficients for test results versus logarithm of bacterial contamination. Statistically and clinically significant differences occurred together only for an elevated level of creatine kinase.
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PMID:Effects of bacterial contamination of reagent water on selected laboratory tests. 43 36


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