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)

Thrombotic complications of percutaneous arterial catheterization still remain a significant and serious problem in infants and children. Systemic heparinization has been recommended for prevention of these complications. The purpose of this study was to evaluate the effect of intraarterial injection of heparin in reducing thrombotic complications following percutaneous femoral artery catheterization. One hundred sixteen consecutive patients (ages four months to 20 years) studied by the Desilets-Hoffman modification of Seldinger's technique of femoral artery catheterization were randomly allocated to the control or heparin groups using a double-blind technique. At the completion of the catheterization, 0.1 mg/kg of placebo or heparin (1,000 units/ml) was injected into the common iliac artery prior to removal of the catheter and sheath. Segmental plethysmography was performed in both lower extremities prior to and after the catheterization, and a plethysmography index (PI) was calculated. The age and sex distribution, diagnoses, number, type, and site of previous catheterization, hemoglobin, platelet count, the amount of flush solution and the heparin contained therein, size of the catheter and sheath used, number of arterial punctures, and the length of the time in the artery were similar in the two groups (P greater than 0.1). Thrombin time and activated partial thromboplastin time were measured prior to the use of flush solution and prior to angiography, and these remained essentially unchanged in the two groups. The PI in the control group (97.5 +/- 320 was not significantly different (P greater than 0.1) from that of the heparin group (97.7 +/- 32). Similarly, the six to 24 month of postcatheterization plethysmography data show no differences (P greater than 0.1). The number of patients with reduced ipsilateral posterior tibial and dorsalis pedis pulses was also similar (P greater than 0.1). None of the patients in either group required thrombectomy. The low low incidence of arterial complications in our patients when compared with other studies may be related in part to the use of a sheath, which is not called for in original Seldinger technique. The data suggest that full-dose heparin administration does not significantly alter arterial complications following percutaneous femoral artery catheterization, especially in children over five years of age.
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PMID:Effect of intraarterial injection of heparin on the complications of percutaneous arterial catheterization in infants and children. 702 38

Histological changes of ligated vasa ovarica, uterina, plica lata, mesosalpinx, mesovarium etc. were studied in 30 women. Thrombus formation, damage of the vessel wall, endothelial cell and tissue bleeding was observed after 30 min. We resected the ligated stumps during the operation, before operation an injection of LMWH was given. No complete, typical occlusive thrombi developed near the ligature. In 3 cases we found evidence of parietal thrombus formation made up of platelets in the art. uterina (10.0%) and in 4 cases in veins, and in a few cases fibrin was present (13.3%). These changes were found in the same number in the vasa ovarica. LMWH reduced the vascular, endothelial damage and the incidence of tissue bleeding. Clinical gynecological experience suggests their safety and effectiveness in thromboprophylaxis. The rapid and direct obliteration of the vascular lumen is due to proliferation of tissue fibroblasts and muscle cells, no bleeding occurred after demarcation of the distal stumps and. LMWH significantly reduces intravasal changes by important intraoperative reactions against thromboplastin generation and haemostasis and can completely replace standard heparin in gynecological prophylaxis.
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PMID:[Removal of the uterus and adnexa and use of low-molecular weight heparin]. 771 99

Heparin is the most frequently used drug for the prevention and treatment of thrombosis. Its use, however, is restricted by its side-effects. To study the efficacy of other glycosaminoglycans that could substitute heparin in the management of arterial thrombosis, 60 guinea-pigs were randomly allocated into 6 groups: G1 = control, G2 = heparin (150 IU/kg), G3 = heparan sulfate from beef pancreas (2.5 mg/kg), G4 = heparan sulfate from beef lung (2.5 mg/kg), G5 = N-acetylated heparan from beef pancreas, G6 = dermatan sulfate from beef intestine (2.5 mg/kg). Ten minutes after intravenous injection of the drugs, thrombosis was induced by the injection of a 50% glucose solution into a segment of the right carotid artery isolated between 2 thread loops during 10 minutes. Three hours later the artery was re-exposed and if a thrombus was present it was measured, withdrawn and weighed. Thrombin time and activated partial thromboplastin time were measured in all animals. Thrombus developed in 90% of the animals in the control group, 0% in G2 and G3, 62.5% in G4, 87.5% in G5 and G6. Only in the animals treated with heparin the coagulation tests were prolonged. In conclusion, in the used dose only the heparan sulfate from beef pancreas presented an antithrombotic effect similar to heparin in this experimental model.
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PMID:Effect of different glycosaminoglycans in a guinea-pig carotid artery thrombosis model. 783 78

A crude, whole-body extract of female heartworms was administered IV to 10 dogs with and 13 dogs without heartworm (HW) infection. Shock developed in 8 of 10 infected dogs and 11 of 13 non-infected dogs, and blood coagulopathy was observed in 12 of 19 dogs with shock. Prevalence and severity of blood coagulopathy were proportionate to prevalence and severity of shock. Platelet count decreased in all dogs with shock with or without blood coagulopathy; thus, the decrease in platelet count might be related to shock. In 4 dogs, activated partial thromboplastin time (APTT) was prolonged--192.0 seconds at 30 minutes after HW injection--and prothrombin time (PT) was increased--13.8 seconds at initial collapse. In 8 dogs, APTT was increased--200 seconds for 2 hours after HW injection--and PT was increased--200 seconds at 30 minutes after the injection. The APTT prolongation might have been caused mainly by decreases in activities of factors VIII, IX, XI, and XII of the intrinsic blood coagulation pathway. In dogs with severely prolonged PT, plasma fibrinogen concentration and factor II activity decreased slightly. Prolonged PT was corrected in vitro by addition of normal plasma at high concentration (> 80%), but prolonged APTT could not be corrected in vitro by addition of 80% normal plasma. Serum fibrin degradation products concentration was < 10 micrograms/ml, and soluble fibrin monomer complex was negative in all dogs. Thrombi were not found in blood vessels of any organ at necropsy and after histologic study. Therefore, it was suggested that blood coagulopathy resulting from inhibition of coagulation factor activities might develop in shock induced by HW extract.
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PMID:Blood coagulopathy in dogs with shock induced by injection of heartworm extract. 787 77

We examined the antithrombotic effect of recombinant human soluble thrombomodulin (rhs-TM) using an arteriovenous shunt thrombosis model and its influence on hemostasis in rats. Intravenous administration of rhs-TM (0.5-4 mg/kg) significantly inhibited thrombus formation and prolonged ex vivo activated partial thromboplastin time (APTT) in a dose-dependent manner. Thrombus formation was inhibited to the same extent in animals treated with heparin (25-200 U/kg) and in those treated with rhs-TM (0.5-4 mg/kg), but heparin had a much stronger effect on prolonging APTT. In the hemorrhagic study using the rat template bleeding time method, rhs-TM exhibited the prolongation of the bleeding time only at the highest effective dose (rhs-TM; 4 mg/kg) of the thrombosis experiments. Thus, rhs-TM exhibits the inhibitory effect on thrombus formation with less APTT prolongation in comparison with heparin and without significant pertubation of hemostasis.
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PMID:Antithrombotic effects of recombinant human soluble thrombomodulin (rhs-TM) on arteriovenous shunt thrombosis in rats. 794 78

The pentasaccharide (PS) comprising the minimal heparin structure capable of binding with antithrombin III (ATIII) and exhibiting anti-factor Xa (anti-fXa) activity in plasma without producing detectable antithrombin activity, has been evaluated for its relative antithrombotic and antihemostatic effects in a baboon model combining both platelet-rich and fibrin-rich thrombosis. Thrombosis was produced in a two-component thrombogenic device incorporated into an exteriorized femoral arteriovenous (AV) shunt in baboons; the proximal component constituted a segment of collagen-coated tubing and induced platelet-rich arterial-type thrombus, while the distal component consisted of an expanded chamber producing static and disturbed flow and initiated fibrin-rich venous-type thrombosis. Thrombus formation was measured as the deposition of 111In-platelets and the accumulation of 125I-fibrin. PS was administered intravenously to maintain plasma anti-fXa activity at three different levels: a) low dose (LD) 0.3 +/- 0.1 U/ml; b) intermediate dose (ID) 0.6 +/- 0.1 U/ml; and c) high dose (HD) 5.6 +/- 0.4 U/ml. In untreated controls, thrombus formed rapidly, reaching a plateau by 40 min of 2.3 +/- 0.2 x 10(9) platelets and 0.62 +/- 0.04 mg fibrin deposited on the collagen segments, and 1.9 +/- 0.4 x 10(9) platelets and 3.3 +/- 0.4 mg fibrin accumulated in the chambers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antithrombotic effects of synthetic pentasaccharide with high affinity for plasma antithrombin III in non-human primates. 811 89

Bay U3405 is a thromboxane A2 (TxA2)-receptor antagonist that inhibits the binding of TxA2 to its target cells. The aim of this study was to determine if Bay U3405 could be used to inhibit arterial thrombosis. A thrombogenic device, consisting of uncrimped Dacron vascular graft material (0.5 cm2) built into the wall of silicone rubber tubing with 4 mm inside diameter, was exposed to native flowing blood under arterial blood flow conditions (100-140 ml/min) by interposing the devices as extension segments into permanent femoral arteriovenous shunts implanted in baboons. Thrombus formation was quantified in vivo by measuring the deposition of 111In-labelled platelets onto the graft material with a scintillation camera. In six baboons, a bolus injection of Bay U3405, calculated to attain an initial plasma concentration of 300 ng/ml, reduced the maximum thrombus formation measured over a 2 h study period. Platelet deposition was reduced by 33 +/- 14% (SD) at 2 h as compared to control studies done in the same baboons. The accumulation of additional platelets onto a thrombus that was allowed to form for 1 h, was reduced by 58 +/- 28% at 2 h. Ex vivo platelet aggregation in response to ADP, activated partial thromboplastin time (APTT), prothrombin time (PT), and thrombin time (TT) were not affected by the treatment. Ex vivo platelet aggregation in response to collagen was markedly inhibited for 2 h after treatment. The results demonstrated that selective blocking of the TxA2-receptor on platelets reduced platelet-dependent thrombus formation and the accumulation of additional platelets in a freshly formed thrombus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vivo inhibition of acute platelet-dependent thrombosis in a baboon model by Bay U3405, a thromboxane A2-receptor antagonist. 811 94

Thrombus formation at a ruptured arterial plaque forming a stenotic luminal outgrowth may trigger acute vascular occlusion. The pathobiology of the complex mechanisms and their interrelationships during this event is not fully understood. However, it is generally believed that components of the subendothelial plaque and the disturbed blood flow conditions caused by the stenosis are of pivotal importance for the thrombus formation. The shape and the severity of the occluding stenosis have profound impacts on the physical aspects of the blood flow. The wall shear rate at the apex may reach extremely high values (> 40,000 s-1). Zones of recirculation proximal and distal to the stenosis as well as turbulent blood flow further downstream from the lesion may occur. The significance of these rheological factors for the mural thrombus formation at various locations at the stenosis is not well established. The extracellular matrix and the cellular components of the subendothelial plaque exposed to the blood stream following plaque rupture are potent inducers of thrombus formation. Matrix components such as collagen fibrils, fibronectin and von Willebrand factor interact specifically with platelet membrane glycoprotein receptors, Ia-IIa, Ib-IX, and IIB-IIa, enabling platelet-subendothelium adhesion, particularly at high wall shear rates. The coagulation cascade is concomitantly activated by the binding of FVII from plasma to tissue factor expressed on the membranes of macrophages and smooth muscle cells. Thrombin, which is subsequently generated at the rupture, enhances the platelet recruitment, and thus the thrombus growth. The thrombin formation simultaneously enhances the deposition of fibrin in and around the platelet masses. Further augmentation of these processes is mediated by the formation of prothrombinase complexes on the phospholipid-rich surfaces of the activated platelets, which increases the local concentration of thrombin at the evolving thrombus. Thrombus fragmentation may represent a serious event, since these fragments may embolize and occlude smaller vessels, producing ischaemia. It is apparent that acute arterial thrombotic occlusion triggered by a ruptured stenotic plaque involves both physical and chemical mechanisms. The inter-relationship and the significance of these complex mechanisms are not well understood. Efficient modalities for therapeutic intervention in thromboembolism at such lesions may not be available before the physical and chemical events are better identified and characterized.
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PMID:Mechanisms of thromboembolism at arterial plaques. 821 59

This study was designed to elucidate the participation of endothelin-1(ET-1) in vivo and in vitro coagulation. The microvascular hemodynamic changes in terms of intravascular thrombus formation in rat mesentery induced by the superfusion of ET-1 (0.5, 1 and 2 pmol) were visualized by an intravital microscope system assisted by television-video tape recorder system. In addition to vasoconstriction we observed the blockade of circulation by clumps resembling thrombus in a dose dependent fashion by ET-1. Thrombus formation could be attenuated by pretreatment with superfusion of 3.8% Na citrate solution but not by the prior superfusion of 1 to 3 ng of nitroglycerine. Thrombus formation was found after the administration of 10 microliters of CaCl2 (100 nM) solution in Na citrate (3.8%, 20 microliters) and ET-1 treated field. In vitro study, a dose dependent increase in TAT (thrombin-antithrombin complexes) and decrease in AT III (antithrombin III) (%) activity, the prolongation of PT (prothrombin time) and APTT (activated partial thromboplastin time) was found by administering ET-1 immediately in native (unanticoagulated) blood in silicon coated test tubes (p < 0.05; n = 6). However in citrated blood, TAT complexes, AT III (%) activity, PT and APTT were not significantly changed after administration of the same doses of ET-1 (p > 0.05; n = 6). Therefore, this study suggested that endothelin-1 caused intravascular thrombosis and enhanced intra test tube coagulation which could be attenuated by blocking ionic calcium.
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PMID:Coagulation in vivo microcirculation and in vitro caused by endothelin-1. 830 59

Factor Xa is a central procoagulant enzyme, linking the intrinsic and extrinsic activation mechanisms to the final common pathway of coagulation. To assess its contribution to pathologic thrombosis, studies were performed in a canine coronary thrombosis model. Thrombus formation was initiated by the application of electric current via a needle electrode placed in the lumen of the left circumflex coronary artery. When 50% occlusion of the vessel developed, the current was stopped and animals received an intravenous bolus of either saline, bovine glutamyl-glycinyl-arginyl-factor Xa (Xai), a competitive inhibitor of factor Xa assembly into the prothrombinase complex, Factor X, or heparin. Animals infused with saline or factor X (300 micrograms/kg) developed total occlusion of the vessel due to a fibrin/platelet thrombus in 70 +/- 11 minutes (36 of 36 animals) and 74 +/- 13 minutes (8 of 8 animals), respectively. In contrast, infusion of Xai prevented thrombus formation completely at a dose of 300 micrograms/kg (8 of 8 animals). As the dose of Xai was decreased, its antithrombotic effect was diminished, with a patency rate of only 2 of 6 animals at a dose of 90 micrograms/kg. Xai at 300 micrograms/kg prevented the accumulation of 125I-fibrinogen/fibrin at the site of the coronary thrombus by approximately 63% and decreased deposition of 111In-labeled platelets by approximately 57%. Hemostatic parameters of animals infused with Xai demonstrated prolongation of the PT and dose-dependent increased extravascular bleeding tendency. These data indicate that factor Xa has a comparably important role in thrombus formation and extravascular hemostasis, and contrast with previous results in this same animal model in which IXai selectively prevented clotting in the coronary vasculature.
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PMID:Active site-blocked factor Xa prevents thrombus formation in the coronary vasculature in parallel with inhibition of extravascular coagulation in a canine thrombosis model. 847 66


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