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)

Pentosan polysulphate is an heparin analogue which acts via an antithrombin III (AT III) independent pathway. We compared the effect of this drug to that of heparin and AT III infusions in AT III deficient patients. Four patients with AT III congenital deficiency received on three different occasions: (i) an infusion of human AT III concentrate (20 U/kg or 40 U/kg), (ii) an intramuscular injection of pentosan polysulphate (2 mg/kg), (iii) a subcutaneous calcium heparin injection (100 U/kg). AT III infusion inhibits the excessive thrombin generation (46% of inhibition) observed in the plasma of AT III deficient patients during at least 12 hours, but does not modify the factor Xa formation. On the contrary, pentosan polysulphate has a marked effect on both thrombin (62% of inhibition) and factor Xa generation (57% of inhibition) still present 8 hours after injection. Heparin injection has the same effect, more prolonged, as pentosan polysulphate on thrombin generation but is not so effective on impairing factor Xa generation (27% of inhibition). The marked effect of pentosan polysulphate on thrombin and factor Xa generation in these patients is due to its AT III independent mechanism of action.
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PMID:Comparison between the effect of pentosan polysulphate heparin and antithrombin III injections in antithrombin III deficient patients. 257 52

A left ventricular assist device (VAD) with a smooth surface of segmented polyurethane was implanted in five goats for 10-55 days, and plasma levels of fibrinogen (Fg), prekallikrein (PK), fibrinogen, fibrin degradation products (FDP), antithrombin III (AT III), prothrombin time (PT), partial thromboplastin time (PTT), platelet (Pl) count, and platelet aggregation (PlAg) induced by adenosine diphosphate were measured during the experiment. Heparin was administered during surgery and no systemic antithrombotic therapy was given thereafter. Before the third postoperative day (POD), plasma levels of Fg and PK were at their lowest, and increased afterward. Between the second and fifth POD PT and PTT increased to 130-160%, and returned to normal gradually. Plasma FDP appeared on the second POD and reached peak values of 10-40 micrograms/ml on the sixth POD. Platelet and AT III levels showed no uniform tendency, but the rate of PlAg decreased to levels of 6-77% before the fifth POD and remained low at approximately 80%, influenced by the pumping even after the 25th POD. In summary, VADs themselves activated coagulation and induced consumption coagulopathy to some degree. However, most of the parameters returned to normal within 2 weeks.
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PMID:Influences of ventricular assist device pumping on blood coagulation. 259 87

Currently there is little information available about the efficacy of heparin during vascular surgery or of the effects of surgical trauma on heparin kinetics. This study was undertaken to evaluate the kinetics of heparin therapy during vascular surgery. Nine patients undergoing major vascular surgery (one carotid, one common iliac and seven aortic operations) were studied both preoperatively and intra-operatively, each patient acting as his own control. Following determination of control activated partial thromboplastin time (APTT) and plasma heparin levels, heparin (100 u/kg body weight) was administered intravenously. Heparin dosage ranged form 4500 units to 8600 units with a mean dose of 6500 units. Plasma heparin and APTT levels were then measured at 10 minute intervals for 1 hour and 20 minute intervals for a second hour. The mean pre-operative and intra-operative APTT levels at ten minutes attained maximal values of 6.6 +/- 3.7 and 8.8 +/- 1.7 times the control respectively. At the end of 2 hours the mean APTT remained greater than 2.5 times the control in both groups. Mean plasma heparin level was 0.83 +/- 0.04 units at 10 minutes and was almost identical in both groups. Heparin level was not a reliable indicator of anticoagulant effect as most patients achieved the same levels but had markedly differing APTT results. The results of this study suggest that excessive doses of heparin may be used in vascular surgery and that surgical trauma does not significantly alter sensitivity to heparin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heparin kinetics in vascular surgery. 262 59

Adequate anticoagulation treatment in patients with deep vein thrombosis reduces the risk of thrombus extension or embolization to less than 5%. Thrombolytic treatment may possibly prevent subsequent postthrombotic syndrome. Heparin is the initial treatment of choice for most patients with deep vein thrombosis. The dose is adjusted according to the results of tests such as the whole blood clotting time, thrombin clotting time, activated partial thromboplastin time or plasma heparin concentration. The most commonly used test is the activated partial thromboplastin time which should be maintained at 1 1/2 to two times the control level. Initially the test should be performed two to three times daily and when optimal adjustment has been established, clotting studies are required only at 24-hour intervals. In general, treatment with intravenous heparin should be continued for seven to ten days. Thereafter, for secondary prophylaxis, treatment with oral anticoagulants is carried out for six to eight weeks for symptomatic lower leg thrombosis, for twelve weeks in the case of proximal venous thrombosis and pulmonary embolism. Oral anticoagulant therapy with warfarin should be given overlapping the last few days of heparin with the dose adjusted to prolong the prothrombin time to 1.3 to 1.5 times control. Initially, the prothrombin time should be monitored weekly, thereafter at intervals of two to three weeks. If oral anticoagulant therapy is contraindicated, secondary prophylaxis with subcutaneous heparin given twice daily in doses sufficient to prolong the activated partial thromboplastin time to 1 1/2 times control is an effective and safe alternative. The major side effect of oral anticoagulant therapy, as well as that of heparin, is bleeding.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Therapy of deep vein thrombosis. 269 42

Heparin and heparin fragments in the molecular mass range 1,700-20,000 Da were examined for their ability to accelerate the antithrombin III (AT III)-dependent inhibition of human factor Xa and the prothrombin converting complex (prothrombinase) during human prothrombin activation. The prothrombinase reaction was modeled by a 3-parameter 2-exponential equation to determine the initial rate of prothrombin activation and the pseudo-first order rate constants of inhibition of prothrombinase and in situ generated thrombin activity. The catalytic specific activities of the heparins increased with increasing molecular size for both the inhibition of prothrombinase and factor Xa. A 10-fold increase over the entire Mr range was found. In contrast to results obtained by others (Ellis, V., Scully, M. F., and Kakkar, V. V. (1986) Biochem. J. 233, 161-165; Barrowcliffe, T. W., Havercroft, S. J., Kemball-Cook, G., and Lindahl, U. (1987) Biochem. J. 243, 31-37), all the heparins showed a 5-fold higher rate of inhibition of factor Xa when compared with the inhibition of prothrombinase, indicating that the factor Va-mediated protection of factor Xa from inhibition by AT III/heparin is independent of the molecular size of the heparin. Our original approach has also revealed a hitherto unrecognized phenomenon, namely, in addition to the accelerating effect of the heparins on the rate of formation of the inactive AT III-factor Xa complex, heparins with Mr greater than 4,500 reduce the initial rate of thrombin generation in the presence of AT III in a concentration-dependent way. We hypothesize that the formation of the dissociable ternary AT III-heparin-factor Xa complex results in a (partial) loss of factor Xa activity towards its natural substrate prothrombin.
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PMID:Antithrombin III-dependent anti-prothrombinase activity of heparin and heparin fragments. 272 56

Abnormal antithrombin III (AT III) was found in the plasma of a 31-year-old female who suffered from recurrent thrombotic episodes. Heparin cofactor activity was 28% of normal and undetectable when measured by inhibition of thrombin and factor Xa (F.Xa), while both progressive antithrombin and antifactor Xa activities were normal. The concentration of plasma AT III antigen was 37 mg/dl. Analysis by crossed-immunoelectrophoresis (CIE) in the presence of heparin and affinity chromatography on heparin-Sepharose revealed that the propositus' AT III did not bind to heparin. When heparin cofactor II (HC II) was removed from propositus' plasma, heparin cofactor activity of AT III was not detected. Thus, HC II seemed to account for the plasma heparin cofactor activity found in the presence of thrombin. The patient's parents and three of her brothers demonstrated qualitative abnormality of AT III; heparin cofactor activity was 30-50% of normal levels in the presence of both thrombin and F.Xa. These findings indicate that the propositus' AT III lacks affinity for heparin and the mode of its inheritance seems to be autosomal dominant and, hence, the propositus would be a homozygote. For this variant, the name of AT III Kumamoto is proposed.
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PMID:Homozygous variant of antithrombin III that lacks affinity for heparin, AT III Kumamoto. 274 90

Amounts of human brain thromboplastin that do not stimulate thrombin generation in platelet poor plasma, were shown to advance by about 4 min an explosive formation of thrombin that occurs after recalcification in the presence of blood platelets. This synergistic effect is inhibited by the specific thrombin inhibitor hirudin and mimicked by adding low concentrations (less than 5 nM) of thrombin to platelet rich plasma. It is our conclusion that small amounts of thrombin, generated under the influence of thromboplastin induced procoagulant activity in the blood platelets. This activity is most likely mainly due to procoagulant phospholipids. Heparin inhibits this effect and retards the explosive thrombin formation. It does not, however, diminish the peak amount of thrombin eventually formed, because heparin neutralizing material released from the activated platelets quenches the heparin effect.
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PMID:The effect of trace amounts of tissue factor on thrombin generation in platelet rich plasma, its inhibition by heparin. 274 91

Heparin has generally been used as an anticoagulant during plasmapheresis. In this study plasma heparin levels were studied in nine patients before double filtration plasmapheresis (DFPP), 30, 60 and 120 minutes after the start of DFPP and at the end of DFPP. Prothrombin time (PT), activated partial thromboplastin time (APTT), bleeding time (BT), plasma fibrinogen levels, FDP and general blood cell examination (CBC) were measured pre and post DFPP. Heparin levels in plasma were lower than 1 (IU/ml) under the dosage of heparin nearly 40 IU/kg/h of heparin administered during DFPP. APTT before DFPP (36.5 +/- 8.2 sec) was nearly double the post-DFPP value (61.4 +/- 12.2 sec). In two patients who were given 30 IU/kg/h of heparin during DFPP, clotting occurred in the DFPP circuit. In conclusion, the optimized dosage of heparin was 40 IU per kg of body weight per hour during DFPP.
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PMID:Optimization of heparinization in clinical double filtration plasmapheresis. 280 1

In 160 high risk patients with total hip replacement the antithrombotic efficacy and tolerance of a single daily injection of 1500 aPTT-U (aPTT = activated partial thromboplastin time) low molecular weight heparin plus 0.5 mg dihydroergotamine (HNMD; Embolex NM) was compared with a twice daily application of 5000 IU of the heparin-dihydroergotamine combination Heparin-Dihydergot in a double-blind study. Deep vein thrombosis measured by means of the radiofibrinogen uptake test occurred in 20.5% of patients in both groups. In addition, intra- and postoperative blood loss and the development of hematoma were similar in both groups. Thus, on account of the "once-daily" application HNMD offers some substantial advantages: The stress of the patient in the postoperative convalescence phase can be appreciably lowered and thereby the nursing staff are spared a great deal of work.
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PMID:Prophylaxis of deep vein thrombosis in high risk patients undergoing total hip replacement with low molecular weight heparin plus dihydroergotamine. 282 40

The assay method of the anti-factor Xa activity of an heparin fragment: the CY 216, is described; it consists of an adaptation of the method of Yin et al. to an automatic clot timer. The anti-factor Xa unit of CY 216 is defined in this assay by comparison to the 4th International Standard of Heparin.
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PMID:[A method of assay of the anti-factor Xa activity of CY 216]. 283 82


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