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)

Prothrombin (factor II) was assayed in a group of coumarin treated patients using the Echis carinatus venom as thromboplastin. The levels obtained were comparable to those observed using the classical one-stage method. A good correlation was in fact observed between the two methods. The levels observed by the Echis carinatus method were definitely lower than those obtained using two immunological methods indicating that Echis carinatus venom activated, in our system, only normal prothrombin. However, even the levels obtained immunologically were slightly decreased, regardless of the method used, as compared to pooled normal plasma. In congenital prothrombin deficiency (homozygotes and heterozygotes) the level obtained by the Echis carinatus method was comparable to that observed by the one-stage method. On the contrary, in a congenital dysprothrombinemia (prothrombin Padua) a normal level was observed whereas the one-stage and two-stage methods yielded constantly levels of about 50% of normal.
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PMID:The "echis carinatus venom" prothrombin assay in coumarin treated patients. A comparison with one-stage and immunological assays. 6 16

A two stage method to determine prothrombin with the chromogenic peptide substrate benzoyl-phe-val-arg-p-nitroanilide has been worked out. Citrated plasma (10 mul) was diluted in 600 mul tris buffer, pH 8.2, ionic strength 0.18 and activated with 250 mul of a commercial rabbit brain-lung thromboplastin. After 325 s incubation at 37 degrees C 200 mul of a 1 mM solution of the chromogenic substrate was added and the increase in absorbance was recorded in a LKB-Beckman 8600 enzyme analyzer. A reading time of 1 minute (including a delay of 20 s) was used which permitted 55 analyses per hour to be carried out. An approximate linear relationship was found between delta A/min and dilutions of normal plasma in prothrombin deficient plasma. The method is insensitive to variations of factors V, VII and X. Less than 10% or normal plasma was needed to "normalize" plasmas deficient in factor V or VII or X. A group of 99 dicoumarol treated patients and 23 normal subjects has been investigated using the present method and compared with a factor II-VII-X determination method. A correlation coefficient of 0.95 was found.
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PMID:Prothrombin determination by means of a chromogenic peptide substrate. 6 99

The adequacy of anticoagulation during 2 hours of cardiopulmonary bypass at 30 degrees C in 9 rhesus monkeys was determined by measuring the whole-blood activated clotting time (ACT) and by noting the appearance of thrombin-altered fibrin (fibrin monomer) and the relative consumption of clotting factors. Factor V and VIII, the heparin cofactor, antithrombin III, prothrombin time, partial thromboplastin time, ACT, platelets, hematocrit, fibrinogen, and fibrin monomer were determined prior to heparinization and after protamine. In 6 of 9 experiments, fibrin monomer became positive in the plasma during cardiopulmonary bypass (CPB), indicating that active coagulation was occurring. In 5 of the 6 animals, initial ACT was less than 400 seconds, and fibrin monomer appeared within the first 30 minutes of bypass. In 1 animal with an initial ACT of 439 seconds, fibrin monomer appeared after 60 minutes of bypass, at which time the ACT was less than 400 seconds. An abnormal level of fibrin monomer was not detected in 5 pediatric patients with an ACT greater than 450 seconds during CPB. Our experimental study and clinical data suggest that the lower limit, as measured by the ACT, for anticoagulant effect to provide coagulation-free CPB is at least 400 seconds.
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PMID:Adequate anticoagulation during cardiopulmonary bypass determined by activated clotting time and the appearance of fibrin monomer. 11 Feb 73

Clotting analysis in 30 patients with bleeding complications in malignant hematological diseases revealed the following troubles: The global tests, Quick's index and partial thromboplastin time markedly differed from normal. Activity of clotting factors revealed hypo- or hyperfibrinogenemia, disturbances of the prothrombin complex (factors II, VII, IX and X), decrease of factors V, VIII, XII. Factor XI (= PTA) was not diminished in any case. Regarding the fibrin-stabilizing factor (factor XIII), its activity was significantly decreased in 30 patients with solid tumors and in 30 patients with hemoblastoses. Faulty clotting balance was characterized by hyperfibrinolysis or disseminated intravascular coagulation (DIC) accompanied by reactive hyperfibrinolysis. About one quarter of the patients with malignant disturbances of the hematopoetic system demonstrated (mostly amegacaryocyte) thrombocytopenia. Finally, treatment of bleeding complications in malignant neoplastic diseases is pointed out.
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PMID:[Hemorrhagic diathesis in patients with malignant neoplasms (author's transl)]. 11 27

Coagulation parameters were studied in rabbits during and after intravenous infusion of suspensions of dispersed fluorochemicals. Blood samples from rabbits given dispersed perfluorobutyltetrahydrofurane or perfluorotributylamine showed thrombocytopenia, prolongation of activated partial thromboplastin time, and decreases in Factors X and XI. The possible presence of an inhibitor of coagulation was suggested by the prolongation of prothrombin time when measured with serial dilutions of thromboplastin reagent. These abnormalities were not found in whole blood or platelet-rich plasma after incubation in vitro with dispersed fluorochemical.
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PMID:Coagulation defects in rabbits after infusion of dispersed fluorochemicals. 12 61

Prekallikrein, plasminogen and prothrombin of human blood plasma have been separately activated by caolin streptokinase and thromboplastin. By measuring the TAME-esterase (N-d Tozy-L-arginine methyl ester) activity of each enzyme and its changes in the course of plasma incubation with the activator, it was possible to estimate the values of precursors of kallikrein, plasmin, thrombin and their inhibitors. Evidence is given that under conditions described the activation is specific of each enzyme and does not affect the level of the two other percursors. The method has been developed in two modifications, permitting to obtain the value of seven parameters in 0.4--0.7 ml of blood plasma.
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PMID:[Method of simultaneous determination of kallikrein, plasmin and thrombin precursors and inhibitors in human blood plasma]. 13 76

Hemostasis was investigated in the postoperative stage (at 24 hours and at 5 days) in 20 patients that had underwent major surgical interventions. The test applied for study of blood coagulation included : thrombocyte counting, the test of Howell, the activated recalcification time, the activated partial thromboplastin time, the prothrombin time (Quick), the thrombin time, estimation of fibrinogen concentration, the protamine sulphate test. The activity of the fibrinolytic system was investigated by the euglobulin clot lysis test and by the method of fibrin plates, while fibrinolysis inhibitors were assessed by determination of serum antiplasmines. Also the fibrinolytic degratation products were evaluated. The results indicate a biological condition that can be classified as "thrombophilia", characterized by hyperfibrinogenemia, the presence of fibrin monomers, a decrease of the fibrinolytic activators and an increase in the amount of antiplasmins, as well as a high percentage of fibrinolytic degradation products. Although the patients did not show manifest signs of thrombosis in the postoperative period, the results obtained indicate a tendency to intravascular formation and deposition of fibrin and suggest the necessity to apply prophylactic therapy with anticoagulants in the postoperative period.
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PMID:[Changes in hemostasis in the postoperative period]. 14 88

alpha(2)-Plasmin inhibitor (alpha(2)PI) is a recently characterized, fast-reacting plasmin inhibitor in human plasma that appears to play an important role in regulation of in vivo fibrinolysis. We report here a case of complete deficiency of alpha(2)PI in man. The patient, a 25-yr-old Japanese man, had a life-long severe bleeding tendency (hemarthrosis and excessive bleeding after trauma). The following tests were within normal limits: platelet count, bleeding time, thrombin time, prothrombin time, partial thromboplastin time, titers of known clotting factors, platelet glass bead retention, Factor VIII-related antigen, platelet aggregation by ADP, collagen and ristocetin, and clot retraction. Routine liver function tests were also normal. The only abnormal finding was that whole blood clot lysis was extemely rapid and was complete in 4-8 h. The concentration of plasma protease inhibitors, including alpha(2)-macro-globulin, antithrombin III, alpha(1)-antitrypsin, and C1INH, were all normal. The concentration of alpha(2)-PI in the patient's plasma, assayed by immunological methods, was <0.1 mg/100 ml (normal concentration, 6.1+/-0.88 mg/100 ml [mean+/-SE]) and functional assays showed a complete deficiency of alpha(2)PI. Addition of purified alpha(2)PI to the patient's whole blood completely corrected the accelerated fibrinolysis. The patient's parents, four siblings, and four other members of this family were asymptomatic, but the titers of alpha(2)PI in their plasmas were congruent with50% of normal pooled plasma. There were three consanguineous marriages in this family, and the alpha(2)PI deficiency appears to have been inherited as an autosomal recessive trait. We speculate that alpha(2)PI deficiency in this patient has led to uninhibited in vivo fibrinolysis that probably causes the severe hemorrhagic tendency. Thus, this study indicates the important role of alpha(2)PI in hemostasis.
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PMID:Congenital deficiency of alpha 2-plasmin inhibitor associated with severe hemorrhagic tendency. 15 96

Plasmin does not activate factor X into the enzyme--factor Xa. On the contrary, the enzyme inactivates factor X, rendering it incapable of conversion into factor Xa during incubation in 25% sodium citrate. After proteolysis by plasmin the prothrombin preparations contaminated with factor X lose their ability to generate thrombin. This ability is partially restored by an addition of factor X.
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PMID:[Inactivation of factor X by plasmin]. 15 77

A study was undertaken to assess the effect of natural oestrogen on the coagulation profile of menopausal women. Forty-five postmenopausal women were selected at random and treated with conjugated oestrogen (PREMARIN) FOR ONE YEAR. Blood samples were tested before treatment, at the end of 3 and 9 months' therapy, and 1 month after treatment had been suspended. Parameters studied included: fibrinogen; platelet count and aggregation; single-stage prothrombin time; kaolin partial thromboplastin time; factors v and x assays and euglobulin lysis time. The only statistically significant alteration noted was a depressant effect on the platelet count. The significance of this change is commented upon. For practical purposes, it may be concluded that treatment of a group of menopausal women with conjugated oestraogen for one year had no adverse effect on their coagulation mechanism.
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PMID:The effect of natural oestrogens on coagulation. 16


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