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)

Eighty patients undergoing total hip replacement (THR) were randomly allocated to three groups. Group I (n = 29) received general anaesthesia, Group II (n = 29) epidural anaesthesia and Group III (n = 22) the same epidural as Group II and the same general anaesthesia as Group I but with a lower isoflurane concentration. Prothrombin time (PT), activated thromboplastin time (APTT), fibrinogen (FG), plasminogen (PG), antithrombin III (AT III), protein C (Proc C), alpha-2-antiplasmin (alpha 2AP), Factor VIII coagulating activity (F VIII:C), von Willebrand factor antigen (vWF:Ag), von Willebrand ristocetin cofactor (vWF:Rcof), tissue plasminogen activator (tPA) as antigen and activity were measured before induction (A), at the end of surgery (B), on the first postoperative morning (C) and 7 days postoperatively (D). The most relevant finding was that AT III was equally depressed immediately after surgery in all groups, but returned to normal significantly faster in the epidural group (mean values at C: 96.2% in Group I, 104.1% in Group II, 92.7% in Group III). The faster return to normal of AT III after epidural anaesthesia could be one of the mechanisms responsible for the beneficial effect of this technique on the prevention of thromboembolic complications.
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PMID:Coagulation and fibrinolytic parameters in patients undergoing total hip replacement: influence of the anaesthesia technique. 268 46

We have proposed previously that the steps in coagulation most sensitive to inhibition by heparin are the thrombin-dependent amplification reactions, and that prothrombinase is formed in heparinized plasma only after Factor Xa activates Factor VIII and Factor V. These propositions were based on the demonstration that both heparin and Phe-Pro-Arg-CH2Cl completely inhibited 125I-prothrombin activation for up to 60 s when contact-activated plasma (CAP) was replenished with Ca2+. Furthermore, the addition of thrombin to CAP before heparin or Phe-Pro-Arg-CH2Cl completely reversed their inhibitory effects. Additional support for the above hypotheses is provided in this study by demonstrating that, when the activity of thrombin is suppressed by heparin (indirectly) or by Phe-Pro-Arg-CH2Cl (directly), exogenous Factor Xa reverses the ability of these two agents to inhibit prothrombin activation. Prothrombin activation was initiated by adding Factor Xa (1 nM) or thrombin (1 or 10 nM) simultaneously with CaCl2 to CAP. In the absence of heparin or Phe-Pro-Arg-CH2Cl, prothrombin activation was seen 15 s later in either case. Heparin failed to delay, and Phe-Pro-Arg-CH2Cl delayed for 15 s, prothrombin activation in CAP supplemented with Factor Xa. In contrast, heparin and Phe-Pro-Arg-CH2Cl completely inhibited prothrombin activation for at least 45 s in CAP supplemented with 1 nM-thrombin. Heparin failed to delay prothrombin activation in CAP supplemented with 10 nM-thrombin, whereas Phe-Pro-Arg-CH2Cl completely inhibited prothrombin activation in this plasma for 45 s. These results suggest that in CAP: (1) Factor Xa can effectively activate Factor VIII and Factor V when the proteolytic activity of thrombin is suppressed; (2) heparin-antithrombin III is less able to inhibit Factor Xa than thrombin; (3) suppression of the thrombin-dependent amplification reactions is the primary anticoagulant effect of heparin.
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PMID:Unfractionated heparin inhibits thrombin-catalysed amplification reactions of coagulation more efficiently than those catalysed by factor Xa. 292 7

A procoagulant activity was found in cerebrospinal fluid (CSF) of patients with myelo- or lymphoproliferative diseases on intrathecal therapy with methotrexate, independently of leukaemic CNS involvement. This activity did not correlate with the cell count in CSF and disappeared on storage at -40 degrees C or after filtration with 0.22 nm filters. Dosage of coagulation factors revealed a strong increase in Factor V activity (F. V:C), an increase in Factor VIII procoagulant activity (F. VIII:C) without a correspondent increase in Factor VIII related antigen (F. VIII R:Ag), and an inconstant increase in Factor IX activity (F. IX:C). These activities all disappeared after filtration with 0.22 micron filters but not with 1.2 micron filters. It is concluded that complexes formed by membrane phospholipids and Factor V were responsible for the procoagulant activity lost after storage. The F. VIII and F. IX.-like procoagulant activity was not lost after storage; it was considered unspecific and attributed to thromboplastin-like substances.
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PMID:Spinal fluid procoagulant activity in leukaemic patients treated with intrathecal methotrexate. 311 27

The authors report a comprehensive evaluation of the hemostatic system in eight related patients with hereditary hemorrhagic telangiectasia (HHT). Unlike in previous reports, they could find no evidence for abnormalities in platelet aggregation or for qualitative abnormalities of the Factor VIII complex. The authors did identify a subgroup of the more severely affected patients in whom Factor VIIIc levels were increased, with shortened activated partial thromboplastin times (APTTs) associated with mild elevations of antithrombin III.
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PMID:Hereditary hemorrhagic telangiectasia. A family study. 313 2

Severe hemorrhagic diathesis caused by hemophilia A (factor VIII:C deficiency) was diagnosed in 2 related Quarter Horse colts. Clinical signs consisted of dyspnea and dysphagia attributable to cranial cervical hematoma in one colt and to intra-abdominal hemorrhage resulting in death of the second colt. Factor VIII:C deficiency, a defect of the intrinsic coagulation pathway, is suggested by results of coagulation studies--prolonged activated partial thromboplastin time, normal prothrombin time, and normal primary bleeding time. The diagnosis was confirmed by results of factor VIII:C assays. Hemophilia A is inherited as an X chromosome-linked trait.
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PMID:Hemophilia A in two related quarter horse colts. 313 24

Two aspects of the activation of factor X by the intrinsic clotting pathway have been studied in purified human systems, in the presence of either purified phosphatidylserine:phosphatidylcholine vesicles (PS:PC) or platelets activated with ionophore A23187: (1) the activation of factor VIII by factor Xa and by thrombin, and (2) the activation of factor X by the factor IXa/VIIIa complex. Factor VIII activation by thrombin was unaffected in either rate or extent by the presence of PS:PC or activated platelets. In contrast, factor VIII activation by factor Xa required either PS:PC or platelets. The products of optimal factor VIII activation by the two enzymes, designated factor VIIIa(T) and factor VIIIa(Xa), are kinetically different in the activation of factor X by factor IXa, factor VIIIa(T) being approximately twice as active (in factor X activation) as factor VIIIa(Xa) in the presence of PS:PC or platelets. Factor VIIIa(Xa) can be converted to the more active VIIIa(T) by thrombin treatment, but the activity of factor VIIIa(T) is unchanged by factor Xa treatment. Factor X activation was also studied with optimally activated factor VIIIa(T), in the presence of PS:PC or activated platelets, as a function of factor IXa concentration in order to determine the apparent dissociation constant for the factor IXa-VIIIa interaction in the two cases. Activated platelets increased the apparent affinity more than fivefold.
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PMID:A comparison of phospholipid and platelets in the activation of human factor VIII by thrombin and factor Xa, and in the activation of factor X. 314 Sep 13

The effect of Norplant subdermal implants on 22 different hemostatic variables was determined in 100 women attending the Fertility Control Clinic of the Singapore National University Hospital before and after 6 and 12 months of use. The factors analyzed were: hematocrit, hemoglobin (Hb), prothrombin time (PT), activated partial thromboplastin time (APTT), platelet count, fibrinogen, coagulation factor II, Factor V,Factor VII, Factor VIII, Factor VIIIR:Ag, Factor X, plasminogen activator, FDP, plasminogen (imm), antithrombin III (functional), antithrombin (antigen), protein C, alpha2-antiplasmin, alpha2-macroglobulin, alpha2-antitrypsin, platelet count, platelet aggregation (ADP), and platelet aggregation (collagen). The factors that differed significantly after 12 months were: Hb,PT,APTT, Factors II,V,VII, and VIIIR:Ag, Plasminogen (imm), antithrombin III(antigen), alpha2-antiplasmin, platelet count, and platelet aggregation. Most of these differences, while significant, were still within the normal range, except for PT,APTT, and platelet count. The subjects were considered to be in an enhanced risk for hypercoagulation and thrombosis.
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PMID:The effects of Norplant-2 rods on clinical chemistry in Singaporean acceptors after 1 year of use: haemostatic changes. 314 69

Platelet fatty acids, platelet aggregations, and coagulation factors were measured in 27 rural blacks, 27 urban blacks and 39 urban whites. Platelets were significantly less aggregable to collagen and arachidonic acid in in both black groups as compared to whites (p less than 0.01), but there were no significant differences in ADP or epinephrine aggregation between these groups. Factor VIII coagulant activity was much higher in rural and urban blacks than whites (p less than 0.001), and the partial thromboplastin times were shorter (p less than 0.005). Platelet arachidonic acid showed a marked difference between the groups, being 16.4 +/- 5.4% of total platelet fatty acids in the rural blacks, 19.9 +/- 4.2% in the urban blacks and 22.6 +/- 3.3% in the whites (p less than 0.001). Whites had higher LDL and lower HDL cholesterol than blacks (p less than 0.005). These findings suggest that in addition to the well known association of raised LDL cholesterol and acute myocardial infarction, platelet aggregation patterns and platelet arachidonic acid levels may be associated risk factors in coronary thrombosis.
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PMID:Platelet aggregations, fatty acids, clotting factors and serum lipids in rural and urban blacks, and urban whites in South Africa. 317

An evaluation of the effect of plasma microparticles (MP) on in vitro coagulation has been undertaken using platelet rich (PRP), platelet poor (PPP) and platelet free (PFP) plasmas prepared by differential centrifugation. MP provide coagulant material which shortens the activated partial thromboplastin time (APTT) and dilute simplastin time (DSTT) which is different from that contributed by commercial phospholipid preparations. The amount of platelet factor three (PF3) available in plasma is directly correlated with the centrifugal force used in its preparation and is present in large amounts in the MP pellet remaining after preparation of PFP. Factor VIII (F.VIII:C) and von Willebrand factor (vWf) were associated with the MP fraction but could be separated from MP on sucrose gradients. The effect of MP on the APTT was independent of the F.VIII:C/vWf and was not solely due to their PF3 content. Plasma prepared for routine coagulation assays contains MP which contribute to the APTT and DSTT and should be considered in their assessment. High speed centrifugation of plasma reduces the F.VIII:C/vWf:Ag/RCoF levels and this may contribute to losses of these proteins during preparative procedures utilising high speed centrifugation.
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PMID:Coagulation activities of plasma microparticles. 326 Oct 52

Packs of fresh-frozen plasma (FFP) from the same donor units were thawed at 37 degrees C and at 45 degrees C in order to determine the suitability of the higher temperature for thawing FFP. Measurements of prothrombin time, activated partial thromboplastin time, fibrinogen concentration, and Factor VIII activity showed no significant differences between the temperatures. Thawing time at 45 degrees C was approximately half that at 37 degrees C. The protocol for manipulation and inspection of the FFP was an important determinant of the thawing time, but did not appear to affect coagulation. FFP can safely be thawed in a 45 degrees C water bath if it is removed before thawing is complete.
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PMID:Thawing of fresh-frozen plasma at 45 degrees C versus 37 degrees C. Comparison using satellite packs of the same donor units. 334 73


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