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Thrombin Hemostatic

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1081. Reduced Platelet Thromboxane Formation in Uremia. EVIDENCE FOR A FUNCTIONAL CYCLOOXYGENASE DEFECT (Full text)

Reduced Platelet Thromboxane Formation in Uremia. EVIDENCE FOR A FUNCTIONAL CYCLOOXYGENASE DEFECT A qualitative platelet abnormality and a bleeding tendency are frequently associated with renal failure and uremia. We demonstrated previously that uremic patients display an abnormal platelet aggregation to arachidonic acid and reduced malondialdehyde production in response to thrombin and arachidonic acid. The objectives of this investigation were: (a) to compare platelet prostaglandin (PG (...) ) and thromboxane (TX) production in whole blood and in platelet-rich plasma (PRP) of 21 uremic patients and 22 healthy subjects; (b) to evaluate the concentration and activity of platelet PG- and TX-forming enzymes; (c) to assess the functional responsiveness of the platelet TXA(2)/PGH(2) receptor; (d) to explore the hemostatic consequences of partially reduced TXA(2) production.Platelet immunoreactive TXB(2) production during whole blood clotting was significantly reduced, by approximately 60%, in uremic

1983 Journal of Clinical Investigation PubMed abstract

1082. A review of alternative approaches in the management of iatrogenic femoral pseudoaneurysms. (Full text)

A review of alternative approaches in the management of iatrogenic femoral pseudoaneurysms. 11041052 2000 10 25 2018 11 13 0035-8843 82 5 2000 Sep Annals of the Royal College of Surgeons of England Ann R Coll Surg Engl A review of alternative approaches in the management of iatrogenic femoral pseudoaneurysms. 364 Sabharwal T T eng Comment Letter England Ann R Coll Surg Engl 7506860 0035-8843 0 Hemostatics EC 3.4.21.5 Thrombin IM Ann R Coll Surg Engl. 1999 Jul;81(4):226-34 10615187 Aneurysm (...) , False drug therapy Femoral Artery Hemostatics therapeutic use Humans Thrombin therapeutic use 2000 10 21 11 0 2001 2 28 10 1 2000 10 21 11 0 ppublish 11041052 PMC2503639 J Vasc Surg. 1997 Jul;26(1):18-23 9240316 J Vasc Surg. 1998 Dec;28(6):1120-1 9917209 J Vasc Surg. 1998 Jun;27(6):1032-8 9652465

2000 Annals of the Royal College of Surgeons of England PubMed abstract

1083. Effects of monoclonal antibodies against the platelet glycoprotein IIb/IIIa complex on thrombosis and hemostasis in the baboon. (Full text)

Effects of monoclonal antibodies against the platelet glycoprotein IIb/IIIa complex on thrombosis and hemostasis in the baboon. To assess the hemostatic consequences and antithrombotic effectiveness of blocking the platelet glycoprotein (GP) IIb/IIIa receptor for fibrinogen and other adhesive glycoproteins in vivo, well characterized murine monoclonal antibodies against the platelet GP IIb/IIIa complex, AP-2 and LJ-CP8, were infused intravenously into baboons. Four animals each received doses (...) of 0.2, 0.4, and 1.0 mg/kg of purified AP-2 IgG, and three animals were given 1.0 mg/kg of the F(ab)2 fragment of AP-2. Five additional animals were given 10 mg/kg LJ-CP8 IgG. At the highest dose, radiolabeled AP-2 IgG bound to an average of 33,000 sites on the circulating platelets. Serial measurements included platelet count, bleeding time, platelet aggregation (induced by ADP, collagen, and gamma-thrombin), and 111In-platelet deposition onto Dacron vascular grafts. Bleeding times were markedly

1988 Journal of Clinical Investigation PubMed abstract

1084. The activation of factor X and prothrombin by recombinant factor VIIa in vivo is mediated by tissue factor. (Full text)

The activation of factor X and prothrombin by recombinant factor VIIa in vivo is mediated by tissue factor. The human coagulation system continuously generates very small quantities of Factor Xa and thrombin. Current evidence suggests that basal level activation of the hemostatic mechanism occurs via Factor VIIa-dependent activation of Factor X, but direct proof has not been available for the participation of tissue factor in this pathway. To examine this issue, we infused relatively high (...) proof will require studies in hemophilic animals using relevant hemostatic endpoints.

1993 Journal of Clinical Investigation PubMed abstract

1085. A unique property of a plasma proteoglycan, the C1q inhibitor. An anticoagulant state resulting from its binding to fibrinogen. (Full text)

no alpha-polymer formation. The anticoagulant effect was undiminished by its binding to C1q, by increased ionic strength, and by CaCl2, but was abolished by incubation of C1qI with chondroitinase ABC. 125I-labeled C1qI bound to immobilized fibrinogen, fibrin monomer, fibrinogen plasmic fragments D1 and E, and fibrin polymers. Occupancy on the E domain required uncleaved fibrinopeptides together with another structure(s), and it did not decrease binding of thrombin to fibrinogen. Occupancy on the D (...) provides dense anchoring of thrombus, substantially enhancing its hemostatic function.

1994 Journal of Clinical Investigation PubMed abstract

1086. Studies of Factors V and VIII:C in an animal model of disseminated intravascular coagulation. (Full text)

of fibrinogen and Factors V and VIII, and a bleeding diathesis developed. Assays of Factors V and VIII were performed by a one-stage prothrombin time and activated partial thrombin time system, respectively. In additional experiments, the effect of the same dose combination of Factor Xa/PCPS on Factor V kinetics was studied by preinfusing 125I-labeled Factor V. After Factor Xa/PCPS infusion, Factors VIII and V were reduced at 2 min by 90 and 50% of the preinfusion levels, respectively, and at 1 h by 80 (...) of DIC. This was confirmed by performing two-stage assays of Factors V and VIII, whereby each was completely converted to the active cofactor, i.e., Va and VIII:Ca, by preincubation of the test sample with thrombin before assaying in a one-stage system as before. The Factor V levels assayed by the two-stage procedure did not change appreciably over 1 h. The Factor VIII levels fell but corrected within 1 h at a time when the level measured by a one-stage assay remained depressed. These results

1984 Journal of Clinical Investigation PubMed abstract

1087. Plasmin inhibition of platelet function and of arachidonic acid metabolism. (Full text)

Plasmin inhibition of platelet function and of arachidonic acid metabolism. To study interactions between platelets and the fibrinolytic system, we examined the effects of human plasmin on human platelets washed by gel filtration. Plasmin concentrations that did not affect platelet shape change, release, or aggregation (less than 1.0 caseinolytic units [CU]/ml) caused a dose- and time-dependent inhibition of platelet aggregation in response to thrombin, ionophore A23187, and collagen. Complete (...) loss of aggregation occurred at 0.1-0.5 CU/ml of plasmin. In a parallel dose-dependent manner, plasmin likewise inhibited thrombin, ionophore, and collagen-stimulated thromboxane B2 production. In contrast, neither aggregation nor thromboxane B2 formation induced by arachidonate was inhibited by plasmin pretreatment of the platelets. Plasmin blocked the thrombin-induced release of [3H]arachidonic acid from platelet membrane phospholipids and the thrombin-induced platelet oxygen burst. However

1985 Journal of Clinical Investigation PubMed abstract

1088. Inflammatory response to cardiopulmonary bypass. (Abstract)

Inflammatory response to cardiopulmonary bypass. Inflammation in cardiac surgical patients is produced by complex humoral and cellular interactions with numerous pathways including activation, generation, or expression of thrombin, complement, cytokines, neutrophils, adhesion molecules, mast cells, and multiple inflammatory mediators. Because of the redundancy of the inflammatory cascades, profound amplification occurs to produce multiorgan system dysfunction that can manifest as coagulopathy (...) of the protease-activated receptor (aprotinin), inhibiting complement-mediated injury (pexelizumab), or inhibiting contact activation (kallikrein inhibitors). Surgery alone also activates specific hemostatic responses, activation of immune mechanisms, and inflammatory response mediated by the release of various cytokines and chemokines. Novel agents are under investigation to further improve outcomes in cardiac surgical patients.

2003 Annals of Thoracic Surgery

1089. Quality of intraoperative autologous blood withdrawal used for retransfusion after cardiopulmonary bypass. (Abstract)

for hemostatic and inflammatory markers were taken from the pooled blood immediately before it was returned to the patient.There was some activation of platelets in the stored autologous blood, as measured by an increase of beta-thromboglobulin. Indications of thrombin formation, as assessed by plasma levels of thrombin-antithrombin complex and prothrombin fragment 1.2 were not seen, and there was no fibrinolytic activity. The red blood cells remained intact, indicated by the absence of plasma free

2003 Annals of Thoracic Surgery

1090. Left atrial appendage function and abnormal hypercoagulability in patients with atrial flutter. (Abstract)

Left atrial appendage function and abnormal hypercoagulability in patients with atrial flutter. The prevalence of thromboembolism might be higher than previously recognized in patients with atrial flutter (AFL) based on findings of transesophageal echocardiography (TEE). To evaluate the potential prothrombotic state in patients with AFL, TEE findings and hemostatic markers were compared among patient groups with AFL, normal sinus rhythm (NSR) and chronic nonvalvular atrial fibrillation (AF (...) ).Cross-sectional study at a university hospital.In 28 patients (mean age, 63 years) with AFL, 58 patients (mean age, 66 years) with AF, and 27 patients (mean age, 61 years) with NSR who underwent TEE, plasma levels of markers for platelet activity (platelet factor 4 and beta-thromboglobulin [beta-TG]), thrombotic status (thrombin-antithrombin III complex and prothrombin fragments 1 and 2) and fibrinolytic status (d-dimer and plasmin-alpha(2)-plasmin inhibitor complex) were determined.Left atrial

2003 Chest

1091. Influence of factor VIIa and phospholipids on coagulation in "acquired" hemophilia. (Abstract)

and increased thrombin generation. No correction of clot formation or thrombin generation was observed when rFVIIa and phospholipids were added to AHBB in the absence of TF.The influence of rFVIIa is dependent on TF, and phospholipids substantially increase the hemostatic (or thrombotic) potential of rFVIIa/TF. (...) Influence of factor VIIa and phospholipids on coagulation in "acquired" hemophilia. This study was performed to evaluate the influences of phospholipids and recombinant factor VIIa (rFVIIa) on thrombin generation and clot formation in "acquired" hemophilia B.A synthetic mixture corresponding to hemophilia A (SHA) and "acquired" hemophilia B blood (AHBB) manufactured in vitro by an anti-FIX antibody were used in this study. With 10 pmol/L tissue factor (TF), 10 nmol/L rFVIIa, and saturating

2003 Thrombosis and Vascular Biology

1092. Analysis of coagulation cascade and endothelial cell activation during inhibition of vascular endothelial growth factor/vascular endothelial growth factor receptor pathway in cancer patients. (Abstract)

Analysis of coagulation cascade and endothelial cell activation during inhibition of vascular endothelial growth factor/vascular endothelial growth factor receptor pathway in cancer patients. The angiogenesis inhibitor SU5416 is a potent inhibitor of vascular endothelial growth factor (VEGF) receptor-1 and -2. VEGF may be involved in hemostasis by altering the hemostatic properties of endothelial cells. We analyzed the effects of SU5416 on the coagulation cascade and the vessel wall in patients (...) with advanced cancer.Markers for thrombin generation, activation of the protein C pathway, fibrinolysis, and endothelial cell activation were measured in patients with renal cell carcinoma, soft tissue sarcoma, or melanoma on days 0, 14, and 28 of treatment with SU5416. Three of 17 sampled patients developed a thromboembolic event in the fifth week of treatment. Markers for thrombin generation and fibrinolysis did not show significant changes. We observed a significant increase in endogenous thrombin

2002 Thrombosis and Vascular Biology

1093. Infection and inflammation and the coagulation system. (Abstract)

Infection and inflammation and the coagulation system. Severe infection and inflammation almost invariably lead to hemostatic abnormalities, ranging from insignificant laboratory changes to severe disseminated intravascular coagulation (DIC). Systemic inflammation results in activation of coagulation, due to tissue factor-mediated thrombin generation, downregulation of physiological anticoagulant mechanisms, and inhibition of fibrinolysis. Pro-inflammatory cytokines play a central role

2003 Cardiovascular Research

1094. Platelet and fibrinogen turnover at the exposed subendothelium measured over 1 year after a balloon catheter de-endothelializing injury to the rabbit aorta: thrombotic eruption at the late re-endothelialization stage. (Abstract)

Platelet and fibrinogen turnover at the exposed subendothelium measured over 1 year after a balloon catheter de-endothelializing injury to the rabbit aorta: thrombotic eruption at the late re-endothelialization stage. Balloon catheter de-endothelialization of the rabbit aorta in vivo causes a rapid release of thrombin and a consequent hemostatic response at the surface of the exposed subendothelium. Previously, we have compared the net fluxes of several hemostatic proteins from plasma

2002 Atherosclerosis

1095. Markers of coagulation and angiogenesis in cancer-associated venous thromboembolism. (Abstract)

Markers of coagulation and angiogenesis in cancer-associated venous thromboembolism. We sought to determine whether venous thromboembolism in cancer patients is associated with aberrant plasma levels of hemostatic and angiogenic factors.Peripheral blood was collected before anticoagulant therapy from cancer patients with acute deep venous thrombosis (DVT; DVT + cancer group, n = 32), those without DVT (cancer control group, n = 36), and patients with acute DVT but no cancer (DVT control group (...) , n = 58). Plasma assays of activation and inhibition of coagulation and fibrinolysis, as well as angiogenesis activation, were then performed.Median levels of thrombin-antithrombin complex, prothrombin fragments 1 + 2, and von Willebrand factor antigen were significantly greater in the DVT + cancer group than in the cancer control and DVT control groups (17.8 ng/mL v 4.6 ng/mL and 9.8 ng/mL, P =.0001 and P =.003, respectively; 3.65 nmol/L v 1.60 nmol/L and 2.71 nmol/L, P <.0001 and P =.011

2003 Journal of Clinical Oncology

1096. Treatment of postcatheterisation false aneurysms: ultrasound-guided compression vs ultrasound-guided thrombin injection (Full text)

of ultrasound-guided compression of iatrogenic femoral pseudo-aneurysms. European Journal of Vascular and Endovascular Surgery 2001;21:248-50. Indexing Status Subject indexing assigned by NLM MeSH Aged; Aneurysm, False /etiology /therapy /ultrasonography; Catheterization, Peripheral /adverse effects; Female; Femoral Artery /injuries /ultrasonography; Hemostatic Techniques; Hemostatics /administration & Humans; Injections, Intralesional; Male; Pressure; Prospective Studies; Thrombin /administration (...) Treatment of postcatheterisation false aneurysms: ultrasound-guided compression vs ultrasound-guided thrombin injection Treatment of postcatheterisation false aneurysms: ultrasound-guided compression vs ultrasound-guided thrombin injection Treatment of postcatheterisation false aneurysms: ultrasound-guided compression vs ultrasound-guided thrombin injection Weinmann E E, Chayen D, Kobzantsev Z V, Zaretsky M, Bass A Record Status This is a critical abstract of an economic evaluation that meets

2002 NHS Economic Evaluation Database. PubMed abstract

1097. Thrombin injection versus compression of femoral artery pseudoaneurysms

, Makaroun M S. Thrombin injection versus compression of femoral artery pseudoaneurysms. Journal of Vascular Surgery 1999; 30(6): 1052-1056 PubMedID Indexing Status Subject indexing assigned by NLM MeSH Adult; Aged; Aged, 80 and over; Aneurysm, False /therapy /ultrasonography; Female; Femoral Artery /ultrasonography; Hemostatic Techniques; Humans; Injections, Intra-Arterial; Male; Middle Aged; Pain Measurement; Pressure; Retrospective Studies; Thrombin /administration & Treatment Outcome; dosage (...) Thrombin injection versus compression of femoral artery pseudoaneurysms Thrombin injection versus compression of femoral artery pseudoaneurysms Thrombin injection versus compression of femoral artery pseudoaneurysms Taylor B S, Rhee R Y, Muluk S, Trachtenberg J, Walters D, Steed D L, Makaroun M S Record Status This is a critical abstract of an economic evaluation that meets the criteria for inclusion on NHS EED. Each abstract contains a brief summary of the methods, the results and conclusions

1999 NHS Economic Evaluation Database.

1098. Efficacy and Safety Study of Fibrin Sealant With 4 IU/mL Thrombin, Vapor Heated, Solvent Detergent Treated (FS VH S/D 4) in Face-Lift Procedures

: Layout table for MeSH terms Thrombin Fibrin Tissue Adhesive Aprotinin Hemostatics Coagulants Trypsin Inhibitors Serine Proteinase Inhibitors Protease Inhibitors Enzyme Inhibitors Molecular Mechanisms of Pharmacological Action (...) Efficacy and Safety Study of Fibrin Sealant With 4 IU/mL Thrombin, Vapor Heated, Solvent Detergent Treated (FS VH S/D 4) in Face-Lift Procedures Efficacy and Safety Study of Fibrin Sealant With 4 IU/mL Thrombin, Vapor Heated, Solvent Detergent Treated (FS VH S/D 4) in Face-Lift Procedures - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save

2008 Clinical Trials

1099. Trial Comparing Outcomes With Merocel Packing or Thrombin-JMI for Anterior Epistaxis

Diseases Otorhinolaryngologic Diseases Hemorrhage Pathologic Processes Signs and Symptoms, Respiratory Signs and Symptoms Thrombin Polyvinyl alcohol formaldehyde foam Formaldehyde Hemostatics Coagulants Disinfectants Anti-Infective Agents (...) Trial Comparing Outcomes With Merocel Packing or Thrombin-JMI for Anterior Epistaxis Trial Comparing Outcomes With Merocel Packing or Thrombin-JMI for Anterior Epistaxis - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved studies (100). Please remove one or more studies before

2008 Clinical Trials

1100. Twice-daily Oral Direct Thrombin Inhibitor Dabigatran Etexilate in the Long Term Prevention of Recurrent Symptomatic VTE

, 2014 Last Verified: February 2014 Additional relevant MeSH terms: Layout table for MeSH terms Thromboembolism Venous Thromboembolism Embolism and Thrombosis Vascular Diseases Cardiovascular Diseases Dabigatran Antithrombins Thrombin Serine Proteinase Inhibitors Protease Inhibitors Enzyme Inhibitors Molecular Mechanisms of Pharmacological Action Anticoagulants Hemostatics Coagulants (...) Twice-daily Oral Direct Thrombin Inhibitor Dabigatran Etexilate in the Long Term Prevention of Recurrent Symptomatic VTE Twice-daily Oral Direct Thrombin Inhibitor Dabigatran Etexilate in the Long Term Prevention of Recurrent Symptomatic VTE - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum

2007 Clinical Trials

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