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)

Heparin and dextran sulfates 8000 are separated from citrated plasma by absorption on epichlorohydrin triethanolamine cellulose columns followed by elution with 1.1 and 1.4 mol/L NaCl in 0.05 mol/L glycine-HCl buffer. The eluate is desalted with Sephadex G25-40, dried, and dissolved in water. A 1 microliters sample is applied to an agarose gel slide. After electrophoresis, the slide is fixed and stained with toluidine blue. The sulfated polysaccharide band(s) is identified by relative electrophoretic migration. The total amount of drug is estimated by matching its optical density with that of a band on one of a set of slides with graded amounts of heparin or dextran sulfate. The reaction with toluidine blue measures the total polyelectrolyte, not just the small proportion of the drug with anticoagulant activity. Pooled normal plasma showed a trace of chondroitin and no heparin. Recovery of heparin and hydrogenated dextran sulfate that was added to pooled normal plasma was complete (lowest concentration tested was 10 micrograms/ml); however, recovery for unhydrogenated dextran sulfate declined consistently by 9 micrograms/ml for concentrations below 50 micrograms/ml, setting a limit for its recovery. Plasma samples taken from patients for coagulation tests were examined by this procedure, and in so doing, steps were ascertained to improve the procedure for routine use. Results were compared with values for prothrombin time and activated partial thromboplastin times obtained on the same samples by the clinical laboratory. Because the procedure provides an independent parameter for measurement in patients who have received heparin therapy, insight into different patient responses to the drug is therefore possible. With minor modifications, the procedure can be used for heparans, dermatans, and chondroitins, because it allows identification and microscale quantitation on the basis of charge, molecular weight, and carbohydrate structure.
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PMID:Determination of absolute amounts of heparin and of dextran sulfate in plasma in microgram quantities. 169 Dec 56

Nonionic radiographic contrast media are used frequently in diagnostic and interventional angiography. However, there is concern that they may possess thrombogenic properties, and some studies have suggested that patients receiving nonionic contrast media are difficult to systemically anticoagulate with intravenous heparin. To investigate the potential effects of nonionic contrast media on systemic anticoagulation during diagnostic cardiac catheterization, pharmacokinetics and in vitro anticoagulant activity following a 3,000 U intravenous heparin bolus were assessed in 12 patients assigned randomly to either an ionic or a nonionic contrast agent. Independent of contrast agent, all patients exhibited biphasic (nonlinear) heparin pharmacokinetics characterized by an initial rapid disappearance phase, followed by a second slower phase. Each patient achieved a therapeutic plasma heparin concentration (greater than or equal to 0.2 U/ml) within 10 min of receiving the bolus, and maintained this level throughout the procedure. Heparin anticoagulant activity, as estimated by a standard activated partial thromboplastin time (APTT) was not affected differently by nonionic as compared with ionic contrast media (p greater than 0.05). Each patient rapidly achieved a level of systemic anticoagulation commonly considered therapeutic (APTT greater than or equal to 1.5 times the control), and maintained this level throughout the procedure. In both groups, APTT correlated directly with plasma heparin concentration (r = 0.95; p less than 0.0001), and inversely with the total amount of contrast media used during the procedure (r = -0.25; p = 0.01). Plasma heparin concentration did not correlate with total contrast media (r = -0.16; p greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heparin pharmacokinetics and in vitro anticoagulant activity in patients receiving nonionic radiographic contrast media. 177 12

Acute paraplegia caused by an epidural hematoma developed in a patient following the removal of an epidural catheter. This catheter had been used for 3 days for postoperative pain relief with no apparent complications. Heparin (10,000 units/day) had been infused for thrombosis prophylaxis and was associated with a normal activated partial thromboplastin time (aPTT) for the first two postoperative days. However, test results from blood drawn prior to catheter removal revealed, in retrospect, an unexpected prolongation of the aPTT (75 s) and PT (56%, Quick's method). An epidural hematoma extending from T12 to L4 was evacuated during emergency laminectomy and neurologic deficits resolved completely over the next days. Thus, the removal of an epidural catheter has the potential for inducing formation of an epidural hematoma. Accordingly, it may be safest to leave epidural catheters in place if test results demonstrate a bleeding diathesis or if a potential for bleeding is suspected on clinical grounds.
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PMID:[Paraplegia following removal of an epidural catheter]. 182

A bolus dose of heparin was administered pre-dialysis to patients (n = 6) undergoing regular maintenance hemodialysis with cuprophane flat plate and hollow fiber membranes. Blood samples were withdrawn at hourly internals for measurement of a) heparin and b) activation markers of coagulation, fibrinolysis and platelets. Two assay methods for heparin were employed; amidolytic assay of anti-factor Xa activity in plasma and a simple whole blood clotting time based upon factor Xa inhibition (Heptest). Results from these heparin assays correlated well with each other (r = 0.89) and both showed similar negative correlations (r = -0.72, amidolytic and r = -0.66, Heptest) with levels of a marker of fibrin clot formation, fibrinopeptide A (FPA). Large differences in levels of FPA were observed during dialysis with the two dialyzer types, when similar levels of heparin were present. Heparin levels declined from 1-5-h dialysis and were associated with rises in plasma levels of FPA, thrombin-antithrombin complex (TAT) and beta thromboglobulin (BTG), but not of D-dimer. Regression analysis revealed the best correlation was between FPA and TAT (r = 0.94), followed by FPA and BTG (r = 0.81). FPA and D-dimer exhibited significant, but lower (r = 0.42), correlation. TAT levels, like FPA levels, showed good correlation with heparin (r greater than 0.65). It is concluded that the Heptest assay may be a useful bedside measurement of heparin levels and the TAT assay may be a simplified means of evaluating coagulation system activation during dialysis.
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PMID:Hemodialysis and heparin. Alternative methods of measuring heparin and of detecting activation of coagulation. 182 95

Angioplasty procedures with balloons, cutters or lasers all may greatly enlarge the arterial lumen, but luminal diameter may decrease because of mural thrombus in 70% to 80%, smooth muscle proliferation, vasoconstriction or recoil. Thrombin binds to arterial wall matrix and fibrin within a thrombus. Heparin dose-dependently decreases platelet and thrombus deposition but does not eliminate these even at high doses. Specific thrombin inhibition started before angioplasty experimentally prevents mural thrombus and limits platelet deposition to a single layer or less. Experimentally, anticoagulant and antifibrin effects occur at lower antithrombin blood levels and lower activated partial thromboplastin times (1.7 times control). Because platelets are so sensitive to thrombin, the higher level of thrombin inhibition required may occur at a specific level (activated partial thromboplastin time greater than or equal to 2 times control); this is not defined in humans. The duration of therapy is not defined in animals or humans. Thrombus and thrombin may be related to cellular proliferation.
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PMID:Importance of antithrombin therapy during coronary angioplasty. 184 31

The indications, efficacy, dosage, administration, and monitoring of heparin and warfarin therapy for acute thromboembolic events are reviewed, with emphasis on recent changes in treatment recommendations. High-dose heparin therapy is indicated for acute deep-vein thrombosis and pulmonary embolism. Heparin therapy as an adjunct to thrombolytic agents for acute myocardial infarction is becoming increasingly accepted. Heparin therapy for acute thromboembolic events consists of a dosage that elevates the activated partial thromboplastin time to 1.5 to 2.0 times the control value; formerly, 1.5 to 2.5 times control was considered therapeutic. The recommended heparin dosage is a bolus dose of 70-100 units/kg followed by an infusion of 15-25 units/kg/hr. To prevent recurrent thromboembolism, most patients require long-term therapy following acute treatment; this typically consists of warfarin, which should be initiated on day 1 or 2 of heparin therapy whenever possible. For most indications, the intensity of warfarin has been reduced to a dosage that elevates the prothrombin time to 1.3 to 1.5 times control. Alternative therapies (low-molecular-weight heparins) and routes (subcutaneous heparin) should be further investigated. Current recommendations for heparin and warfarin therapy of acute thromboembolism include reduced intensity of both drugs and shortened duration of therapy. Since the therapeutic ranges for both heparin and warfarin therapy have been compressed, closer monitoring may be necessary to achieve and maintain adequate anticoagulation.
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PMID:Therapy of acute thromboembolism with heparin and warfarin. 179 18

Heparin is used routinely in the US as adjunct therapy for prevention of reocclusion after thrombolysis during acute myocardial infarction. A review of the literature shows controversy over the efficacy of heparin following thrombolysis. Both beneficial and a lack of beneficial effects have been reported with heparin. From a pathophysiologic viewpoint, there appears to be a need for full heparinization in the postlytic period because the residual stenosis is highly thrombogenic. However, optimal dose, time, and mode of heparin therapy has not been defined. Despite a lack of definitive data, it seems reasonable to administer intravenous heparin immediately after thrombolytic therapy to achieve a partial thromboplastin time 1.5-2.0 times control that is concurrent with an antiplatelet agent such as aspirin. These recommendations are consistent with the consensus opinion of the American College of Cardiology and the American Heart Association.
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PMID:The controversy of heparin therapy as an adjunct to thrombolysis in acute myocardial infarction. 187 72

Heparin and warfarin sodium (Coumadin, Panwarfin, Sofarin) are used most often to treat acute and recurrent venous thromboembolic disease, arterial disease, valvular heart disease, and atrial fibrillation. These agents along with dextran, pneumatic compression devices, and gradient stockings are also used to prevent deep venous thrombosis and pulmonary embolism in patients at high risk (eg, those with venous stasis, lower limb or spinal cord trauma, clotting abnormalities). Anticoagulation therapy is monitored by maintaining the activated partial thromboplastin time and the prothrombin time in the therapeutic range.
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PMID:Using anticoagulants safely. Guidelines for therapeutic and prophylactic regimens. 188 10

Various preparations of heparin from different manufacturers are commercially available. The influence of bovine lung heparin (BLH) and porcine mucosal heparin (PMH) on anticoagulation and heparin plasma concentration was investigated in four groups of 10 patients undergoing elective aortocoronary bypass grafting either after single dose or repetitive dose (after 60 minutes) of one of these heparin preparations. Heparin plasma concentration increased significantly after injection of heparin (BLH: minimum, 1.67 U/mL; maximum, 2.10 U/mL; PMH: minimum, 1.69 U/mL; maximum, 2.15 U/mL). Sixty minutes after the initial dose, heparin plasma levels were higher in the patients who received PMH. Supplemental heparin doses 60 minutes after the loading dose increased plasma heparin concentration only with porcine mucosal heparin. Elimination of heparin in the urine was not different among the groups. Fibrinogen and antithrombin III concentrations, as well as activated clotting time (ACT; always greater than 400 seconds) and partial thromboplastin time (PTT; always greater than 300 seconds), did not differ among the groups, indicating effective anticoagulation during the bypass period with both types of heparin. It can be concluded that sufficient anticoagulation can be achieved with either kind of heparin. PMH seems to be longer acting and a repeat dose in these patients seems to be necessary only if cardiopulmonary bypass lasts longer than 90 minutes.
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PMID:Does the preparation of heparin influence anticoagulation during cardiopulmonary bypass? 193 49

We evaluated the effect of the RGD-containing peptide, echistatin, on thrombolysis time and acute reocclusion in a canine model of coronary thrombosis/thrombolysis. Occlusive thrombus formation was induced by electrical injury, via a stimulating electrode, to the endothelial surface of the circumflex coronary artery in the open-chest, anesthetized dog in the presence of a critical stenosis. Fifteen minutes after occlusive thrombus formation, dogs received either an intravenous infusion of vehicle (saline at 0.1 ml/min) or echistatin (15 micrograms/kg/min i.v.). Heparin was given as an initial bolus (100 U/kg i.v.) 15 min after thrombus formation and repeated at hourly intervals (50 U/kg). This dose of heparin increased activated partial thromboplastin time to 1.5- to 2.5- fold over control. Thrombolysis was induced with recombinant tissue-type plasminogen activator (tPA) at a total dose of 1 mg/kg, intravenously administered over 90 min with 10% given as an initial bolus. The vehicle-treated animals reperfused at 48 +/- 9 min with a reperfusion incidence of 60% (3/5). The echistatin-treated animals reperfused at 46 +/- 5 min with a reperfusion incidence of 100% (5/5). After stopping the tPA infusion, acute reocclusion occurred in 100% (3/3) of the vehicle-treated dogs and in only 20% (1/5) of the echistatin-treated dogs. Echistatin caused a greater than 5-fold increase in buccal mucosa bleeding time and almost completely inhibited ex vivo platelet aggregation to ADP, collagen, and U-46619. Residual thrombus wet weight, determined at the end of the experiment, was significantly lower for the echistatin group (2.1 +/- 0.2 mg) compared to the vehicle group (5.8 +/- 0.7 mg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevention of reocclusion following tissue type plasminogen activator-induced thrombolysis by the RGD-containing peptide, echistatin, in a canine model of coronary thrombosis. 194 98


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