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)

The exposure of rats to 100% oxygen at 1 atmosphere leads to a prolongation of prothrombin times and activated partial thromboplastin times. This development is associated with a consumption of factor XII, VIII, and VII activities and with the appearance of fibrin monomers and fibrinogen degradation products. Lead acetate enhances all oxygen-induced changes of the coagulation systems drastically. The O2 survival time of chicks which are naturally deficient in factor XII is greatly increased over that of rats and is not affected by lead acetate. Oxygen survival times of rats suffering from chronic respiratory disease (CRD) are also significantly increased when compared with normal rats. It appears that consumptive coagulopathy and disseminated intravascular coagulation are early events in oxygen exposure, and that their development is accelerated by lead ions.
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PMID:Oxygen-induced consumptive coagulopathy and its enhancement by lead acetate. 57 13

Blood coagulation and fibrinolysis were assessed in 13 Finnish amateur runners aged 31 to 48, and one 65-year old taking part in a non-competitive marathon (42.2 km). After the run the mean values of partial thromboplastin time showed a very significant shortening, whereas the mean values of the prothrombin time and of plasma fibrinogen were not significantly altered. The mean values of euglobulin lysis time were significantly shorter and the mean values of fibrin degradation products increased highly significantly. After the run, protamine sulphate was positive or strongly positive in all subjects, whereas the ethanol gelation test was negative in all runners; no cryofibrinogen was detected in any participant. Thus, running a marathon race affects the haemostatic balance and activates the fibrinolytic mechanism. The effects of training and physical fitness on the above parameters are discussed.
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PMID:Marathon run I: effects on blood coagulation and fibrinolysis. 57 24

Coagulation and fibrinolysis were studied in a colony of aged Syrian hamsters with spontaneous atrial thrombosis, and the results are consistent with concomitant consumption coagulopathy. In comparison to age- and sex-matched hamsters from the same colony, those with atrial thrombi had significantly prolonged prothrombin and partial thromboplastin times, reduced levels of factors II, VII, VIII and X activities and plasminogen; and concentrations of fibrinogen-fibrin split products in excess of 80 microgram/ml. Hematocrits of the thrombosed animals were significantly decreased, total plasma proteins were increased, leukocyte counts were within normal limits, and platelet counts were about half those of the controls. Thrombosed hamsters had significantly reduced plasma albumin content, increased alpha1-, beta-, and gamma-globulins, and reduced A/G ratios. Aged sick hamsters demonstrable thrombi also had reduced coagulation and fibrinolytic activities and platelet counts, but their fibrinogen levels were markedly elevated, and fibrinogen-fibrin split products were either absent or present in trace amounts. This suggests an earlier and/or less acute form of the thrombotic process.
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PMID:Spontaneous atrial thrombosis in aged Syrian hamsters. II. Hemostasis. 57 88

The medical records of 118 cases who met laboratory criteria of DIC were studied. The most frequent etiologies were: Generalized infection (39.8%), trauma (16.9%), malignancy (6.8%) and surgical cases (6.8%). The main clinical manifestations which appeared to be related solely to DIC were (in a decreasing order of frequency): Bleeding (64.4%), renal dysfunction (24.6%), liver dysfunction (18.6%), respiratory dysfunction (16.1%), shock (14.4%), thromboembolic phenonmena (6.8%) and central nervous system involvement (1.7%). In 26 patients none of these manifestations were observed. In patients with infection, liver and renal dysfunction were frequent and respiratory dysfunction rare, whereas in trauma cases, liver and renal dysfunctions were rare and respiratory dysfunction frequent. This variability indicates that the clinical manifestations are affected not only by the process of intravascular coagulation but also by the underlying clinical disorders. The most impaired coagulation tests were prothrombin time, partial thromboplastin time, platelet count and thrombin time. The degree of abnormality of these coagulation tests was found to be related to the extensiveness of organ involvement. The mortality (overall 54.7%) increased independently with age, with the number of clinical manifestations and with the degree of abnormality of the above-mentioned four most impaired coagulation tests. In addition, older patients were more likely to have an increased number of clinical manifestations and more impaired coagulation tests. Mortality was similar in the various etiologies except for trauma patients in whom it was lower (30%).
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PMID:Clinical and laboratory aspects of disseminated intravascular coagulation (DIC): a study of 118 cases. 58 Apr 88

An improved method for the preparation of bovine alpha-thrombin is described. The procedure involves that activation of partially purified prothrombin with tissue thromboplastin followed by chromatography on Sulfopropyl-Sephadex C-50. The purified enzyme is homogeneous on polyacrylamide discontinuous gel electrophoresis and has a specific activity toward fibrinogen of 2.200-2,700 N.I.H. U/mg. Its stability on storage in liquid media is dependent on both ionic strength and temperature. Increasing ionic strength and decreasing temperature result in optimal stability. The denaturation of alpha-thrombin by guanidine hydrochloride was found to be a partially reversible process with the renatured species possessing properties similar to "aged" thrombin. In addition, the catalytic properties of alpha-thrombin covalently attached to agarose gel beads were also examined. The activity of the immobilized enzyme toward fibrinogen was affected to a much greater extent than was the hydrolysis of low molecular weight, synthetic substrates.
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PMID:On the preparation of bovine alpha-thrombin. 58 Apr 93

10 women with unwanted pregnancies in the first and second trimester were terminated by use of intramuscular injections of 15-Methyl-PGF2alpha. Studies of bleeding and recalcification time, platelet count, levels of heat-fibrin, prothrombin, partial thromboplastin time, platelet adhesiveness and heparinocytes were performed before treatment. 30 minutes, 4 and 8 hours after beginning of 15-Methyl-PGF2alpha-administration, 2 hours after the expulsion of the product of conception and 24 hours after first investigation. Prothrombin decreased during treatment with 15-Methyl-PGF2alpha and did not obtain the starting value 24 hours after first investigation. Platelet count showed an equal attitude. The time of recalcification increased continuous. Heparinocytes continuous decreased up to 2 hours after expulsion of the product of conception. 24 hours after first investigation a significant ascent was noticed. The results of the studies on coagulation did not indicate a strong injury of coagulation system. They suggest the positive estimation of termination of pregnancy in the first and second trimester with 15-Methyl-PGF2alpha.
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PMID:[Blood coagulation studies of therapeutic abortion induced by 15-methyl-prostaglandin F2 alpha]. 60 4

A few neonates born to mothers receiving anticonvulsant drugs during pregnancy have shown defects in vitamin K dependent clotting factors with or without clinical bleeding. Experimentally, phenytoin (diphenyl hydantoin, DPH) has induced clotting defects in cats and inhibited production of clotting factors in rat liver slices. Phenobarbital has produced similar but milder defects. Anticonvulsants have been observed to produce clotting defects in 9 children, 2 weeks to 8 years in age. Elevated levels of phenytoin or other anticonvulsants, or a combination of anticonvulsants were measured in the children. Six patients were on drug combination including two or more of the following: phenytoin, phenobarbital, primidone, carbamazepine, diazepam, ethosuximide. Clotting defects included: elevated prothrombin time, elevated partial thromboplastin time, diminished factors V, VII or X. All children had neurologic symptoms of anticonvulsant toxicity, but the only hematologic problems were oozing from venipuncture sites and increased bruising in 3. All patients were on normal diets and had normal liver function tests. By lowering the level of anticonvulsants, clotting factors returned toward normal. Elevated levels of anticonvulsants can potentially produce clotting defects in neonates and young children.
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PMID:Anticonvulsivant-induced depression of clotting factors in children. 61 36

Autoprothrombin II-A anticoagulant was isolated from bovine prothrombin. Purified prothrombin was applied to DEAE-cellulose chromatography after incubation with thrombin. Four protein peaks were obtained where the third peak corresponded to the anti-coagulant effect. The fractions under the third peak were pooled together and the anticoagulant effect was evaluated with different methods. From 25,470 +/- 2,800 U of prothrombin, 5,800 +/- 1,400 U of inhibitor were obtained. The inhibitor was found to be most effective at pH 7.2--7.8. In vitro, the inhibitor inhibited the thrombin time and the plasma clotting time highly significantly but had no effect on euglobulin lysis time and fibrin plates. In vivo, when injected into rabbits, the inhibitor effect was also significant on the same tests. The autoprothombin II-A anticoagulant had a protective effect on DIC formation with rabbit brain thromboplastin administration. This protective effect was found to be statistically significant.
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PMID:Some properties of autoprothrombin II-A anticoagulant. 61 78

Thrombogenicity of the factor IX concentrate and its clinical use for stoppage of the bleeding in the case of hemophilia A with inhibitor were reported. (1) Factor IX concentrate contained the coagulation factors as prothrombin complex (factors II, VII, IX and X); Thrombin and factor Xa. (2) Prothrombin in the factor IX concentrate could be converted to thrombin without any additional procoagulant such as thromboplastin or factor V, but in just 2.5M glycine solution by the effect of factor Xa. (3) The infusion of factor IX concentrate into a rabbit induced DIC promptly which was proved by autopsy and coagulation-fibrinolytic studies. (4) Factor IX concentrate showed a great efficacy in stopping the bleeding in the case of hemophilia A with inhibitor.
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PMID:Characteristics and thrombogenicity of factor IX concentrate. 61 88

It was found that phosphatidylserine inhibits the activating effect of factors V, VII and autoprothrombin C on the thromboplastin time of plasma. This is in agreement with the previously observed phosphatidylserine ability to form an inactive complex with the substrate of thrombinogenesis, i.e. prothrombin. The excess of autoprothrombin C results in changes in the kinetic parameters of the inhibiting effect of phosphatidylserine on the thrombinogenesis, which is indicative of the interaction between autoprothrombin C and phosphatidylserine. Data from gel-filtration on Sephadex G-100 and differential spectrophotometry support the evidence for the formation of the autoprothrombin C-phosphatidylserine complex. During ion-exchange chromatography and gel-filtration the autoprothrombin C preparations are eluted as an acute symmetrical peak; using electrophoresis in agarose gel, two fractions were revealed in the preparations. The first fraction migrates with gamma-globulins, whereas the second one--with alpha-globulins. The presence of phosphatidylserine in the autoprothrombin C solution does not change its migration rate during electrophoresis.
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PMID:[Effect of phosphatidylserine in hemocoagulating action of factors V, VII and autoprothrombin C]. 62 47


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