Academic literature on the topic 'Anticoagulants Platelet Aggregation'
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Journal articles on the topic "Anticoagulants Platelet Aggregation"
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Gallistl, Siegfried, Gerhard Cvirn, Birgit Roschitz, Martina Petritsch, Bettina Leschnik, Wolfgang Muntean, and Martin Koestenberger. "Combined Effects of Eptifibatide and Anticoagulants: Differences between LMWH and UH or rH in Thrombin Generation Inhibition but not in Platelet Aggregation Inhibition." Thrombosis and Haemostasis 88, no. 12 (2002): 1012–19. http://dx.doi.org/10.1055/s-0037-1613348.
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SummaryAim of our study was to investigate effects of eptifibatide and anticoagulants on platelet aggregation and thrombin generation under low and high coagulant challenge in tissue factor-activated platelet rich plasma using a model allowing simultaneous determination of the time course of platelet aggregation and thrombin generation. Eptifibatide exerted a dose-dependent anti-aggregating effect under both high and significantly stronger under low coagulant challenge. Combination of eptifibatide and anticoagulants resulted in significant additive prolongation of the lag phase until the onset of platelet aggregation, more pronounced under low coagulant challenge. Under high, but not under low coagulant challenge combination of eptifibatide and anticoagulants had a significant synergistic inhibitory effect on platelet aggregation. Under low coagulant challenge combination of eptifibatide with LMWH, but not with UH, or rH, resulted in significantly reduced thrombin potential, F 1+2 generation, and FXa formation compared to measurements in the absence of eptifibatide.We demonstrate a synergistic effect of eptifibatide and anticoagulants on platelet aggregation inhibition and an additional inhibitory effect of LMWH and eptifibatide on thrombin generation. Our results support the notion that combination of eptifibatide and anticoagulants might be beneficial in atherosclerotic disease to palliate the thrombogenic potency of ruptured atherosclerotic plaques.
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Cimminiello, C., M. Milani, T. Uberti, G. Arpaia, and G. Bonfardeci. "Effects of Ticlopidine and Indobufen on Platelet Aggregation Induced by A23187 and Adrenaline in the Presence of Different Anticoagulants." Journal of International Medical Research 17, no. 6 (November 1989): 514–20. http://dx.doi.org/10.1177/030006058901700603.
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As Ca2+ is known to play a fundamental role in platelet function, the effect of combining two platelet aggregating agents (adrenaline and the ionophore A23187) with different effects on Ca2+ was studied at levels subthreshold for aggregation using platelet-rich plasma from eight atherosclerotic patients. Adrenaline lowered the A23187 threshold required to induce aggregation. The effects of treating patients with the antiplatelet agents, indobufen and ticlopidine, on A23187 and adrenaline induced aggregation of platelets prepared in hirudin or sodium citrate was also evaluated. Aggregation was also studied using platelets resuspended in Ca2+-free and Ca2+-enriched Tyrode solution. Before treatment hirudin treated platelet-rich plasma, which has physiological extraplatelet Ca2+ levels, was more sensitive to A23187 and adrenaline than was citrated platelet-rich plasma, which has suppressed Ca2+ levels. Ticlopidine significantly raised the concentration of A23187 required to induce aggregation in citrated but not hirudin treated platelet-rich plasma. Indobufen did not significantly affect A23187 induced aggregation. Ticlopidine acts by inhibiting the glycoprotein IIb – IIIa complex on the platelet membranes. Low levels of extracellular Ca2+ and ticlopidine may act synergistically to reduce the aggregatory response of stimulated platelets.
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Wallén, N. Håkan, Claes Held, Nina Rehnqvist, and Paul Hjemdahl. "Impact of Treatment with Acetylsalicylic Acid on the Proaggregatory Effects of Adrenaline in vitro in Patients with Stable Angina Pectoris: Influence of the Anticoagulant." Clinical Science 85, no. 5 (November 1, 1993): 577–83. http://dx.doi.org/10.1042/cs0850577.
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1. The impact of oral acetylsalicylic acid treatment on the enhancing effect of adrenaline on platelet aggregation in vitro was investigated in patients with stable angina pectoris. In addition, the influence of different anticoagulants (i.e. hirudin and citrate) on platelet aggregation in vitro was compared. 2. Eighty-four patients with stable angina pectoris were studied. Sixteen patients were on acetylsalicylic acid treatment (150-250 mg daily), whereas 68 patients were free from acetylsalicylic acid. Platelet-rich-plasma was prepared from citrate- or hirudin-antkoagulated blood. The EC50 (i.e. the concentration of agonist required to produce half-maximal aggregation) for the ADP-induced extent of aggregation was determined. Thereafter the enhancing effect of adrenaline (10 and 50 nmol/l) on ADP-induced aggregation (at EC50) was investigated. 3. In the patients with angina, acetylsalicylic acid caused the expected effects on ADP-induced platelet responses. Adrenaline significantly enhanced both the extent of aggregation and the initial rate of aggregation (primary aggregation), irrespective of the anticoagulant used. In acetylsalicylic acid-treated patients (citrated platelet-rich plasma) the extent of aggregation was partly inhibited, but no significant effect on the rate of aggregation could be observed. 4. A comparative substudy of the anticoagulants in healthy subjects (n = 8) showed that both the aggregating effect of ADP per se and the enhancing effect of adrenaline on ADP-induced aggregation (at EC50) were less influenced by acetylsalicylic acid when evaluated in hirudinized platelet-rich plasma (i.e. with physiological levels of extracellular calcium) as compared with citrated platelet-rich plasma. 5. It is concluded that acetylsalicylic acid treatment slightly attenuates the proaggregatory effect of high physiological concentrations of adrenaline in vitro. The impact of acetylsalicylic acid in vitro is, however, strongly dependent on the anticoagulant used, and is significantly weaker when evaluated in a medium with normal extracellular calcium levels (i.e. hirudin) than in a medium with low levels of extracellular calcium (citrate). Thus, acetylsalicylic acid may be a weak antagonist of catecholamine-induced platelet activation in vivo.
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Białecka, Monika, Anna Machoy-Mokrzyńska, and Anna Pierzchlińska. "Lumbar puncture in patients on anticoagulants." Aktualności Neurologiczne 20, no. 2 (October 30, 2020): 51–58. http://dx.doi.org/10.15557/an.2020.0007.
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Lumbar puncture is an important invasive procedure often used in the diagnosis of neurological disorders. Generally, lumbar puncture is a safe procedure, with a very low incidence of serious complications, the risk of which, however, may increase in the group of patients on anticoagulant therapy (anticoagulants and platelet anti-aggregation agents). This applies to both the risk of haemorrhagic complications and the risk of thrombotic events during temporary discontinuation of anticoagulants. This paper presents the current knowledge on the management in patients receiving anticoagulants (vitamin K antagonists, new anticoagulants, heparins, fondaparinux) and platelet anti-aggregation agents (P2Y12 platelet receptor antagonists, glycoprotein IIb/IIIa inhibitors, acetylsalicylic acid) who require lumbar puncture. Furthermore, we present the issue of bridging therapy in patients at a high risk of thrombotic complications. In the case of neurological indications for a lumbar puncture in a patient on anticoagulants or anti-aggregation therapy, the urgency of the procedure and the risk of adverse effects should be assessed and other diagnostic methods should be considered in the first place. If there is a need for an urgent lumbar puncture, treatment modification or the use of drugs to reverse the anticoagulant or anti-aggregation effect may be necessary. Each case must be treated individually, considering medical and family history, comorbidities and other medications taken by the patient. Most of the available recommendations related to the presented problem have been developed by anaesthetic associations. There is a need to popularise the principles of management in patients on anticoagulants who require lumbar puncture due to neurological disorders.
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Lewis, Bruce E., Christopher Aranda, Mary Lewis, Debra Hoppensteadt, Jeanine M. Walenga, and Jawed Fareed. "Unlike Heparins Newer Oral Anticoagulants Do Not Interact with HIT Antibodies and Maybe Useful in the Longterm Anticoagulant Management of Heparin Compromised Patients." Blood 118, no. 21 (November 18, 2011): 2317. http://dx.doi.org/10.1182/blood.v118.21.2317.2317.
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Abstract Abstract 2317 Introduction: Heparin and low molecular weight heparins such as enoxaparin and dlateparin are widely used in the management of thrombosis and cardiovascular disorders. However these anticoagulants are capable of producing the generation of HIT antibodies and their use is not recommended in patients with previous history of HIT. More recently several new oral anticoagulants have been approved around the world. These include the oral anti-Xa agents namely, Apixaban (Bristol-Myers Squibb), Rivaroxaban(Bayer Healthcare) and anti-IIa agents, dabigatran (Boehringer-Ingelheim). All of these represent synthetic low molecular weight compounds. Apixaban and Rivaroxaban are active agents where as Dabigatran requires endogenous activation. The purpose of this investigation was to determine the relative effects of the newer anticoagulants and enoxaparin on HIT antibody mediated platelet aggregation and other interactions with platelets. Materials: Rivaroxaban was obtained in powdered form from Bayer Healthcare (Wuppertal, Germany) Apixaban and Dabigatran were of synthetic origin. Enoxaparin was obtained from Sanofi-Aventis (paris, France). All drugs were dissolved in appropriate solutions and a working solution of 100 ug/ml was prepared in buffered saline. Pooled HIT sera was prepared by pooling clinically symptomatic HIT patients with high titers of anti-heparin platelet factor 4 antibodies. Method: Whole blood samples drawn from normal healthy volunteers were supplemented with each of these agents at a graded concentration of 0–100 ug/ml for 60 minutes to determine the relative release of platelet factor 4. To test the interaction of HIT antibody with each of these agents 50 ul of PRP samples were mixed with 150 ul HIT positive heat inactivated sera/plasma or plasmapheresis fliud (collected from symptomatic HIT patients). Graded amounts of each of these new anticoagulants at 0.1, 1.0 and 10 ug/ml were added to test the platelet aggregation response at a period of 60 minutes. Results: In contrast to enoxaparin which produced an increase in the platelet factor 4 release upon 60 minute incubation 25.6+3.1 ng/ml), none of the new oral anticoagulants produced an increase in the PF4 <15.0 ng/ml. Enoxaparin also produced a strong HIT antibody mediated response, whereas none of these newer oral agents produced any aggregation responses. Conclusion: These studies demonstrate that –enoxaparin the newer oral anticoagulant drugs do not interact with HIT antibody to mediate plarelet aggregation responses. Moreover, these newer agents do not promote platelet factor 4 release. Thus, these agents can be used in the long term anticoagulant management of heparin compromised patients. Disclosures: No relevant conflicts of interest to declare.
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Sokolova, N. A., M. I. Savina, and O. S. Shokhina. "EDTA‑dependent pseudothrombocytopenia in child (clinical case report)." Medical alphabet, no. 13 (June 29, 2021): 51–54. http://dx.doi.org/10.33667/2078-5631-2021-13-51-54.
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Ethylenediaminetetraacetic acid (EDTA)-dependent pseudothrombocytopenia is the phenomenon of a spurious low platelet count due to antiplatelet antibodies that cause platelet clumping in blood anticoagulated with EDTA. The aggregation of platelets in EDTA-dependent pseudothrombocytopenia is usually prevented by other anticoagulants, such as sodium citrate. EDTA-dependent pseudothrombocytopenia has never been associated with hemorrhagic diathesis or platelet dysfunction. In this article, a 2,5-year-old boy with EDTA-dependent pseudothrombocytopenia is presented because of rare presentation. We report that EDTA can induce platelet clumping, and thus spuriously low platelet counts. However, aggregation of platelets was not detected in blood samples with sodium citrate, and platelet count was normal.
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Wysokinski, Waldemar, Robert McBane, James H. Chesebro, and Whyte G. Owen. "Reversibility of Platelet Thrombosis In Vivo." Thrombosis and Haemostasis 76, no. 06 (1996): 1108–13. http://dx.doi.org/10.1055/s-0038-1650714.
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SummaryReversibility in vivo of acute platelet thrombosis in response to specific anticoagulants is analyzed with thrombi that develop in segments (1 cm) of porcine carotid arteries externally crushed with a hemostat. Most thrombi fill the lumens of the injured segments (ca. 1 cm × 3 mm, 1 × w) within 30 min and comprise masses of platelets interpenetrated with neutrophil-lined seepage channels of blood. Continuous quantitative assay of thrombus mass is provided by a gamma detector placed over the injured segments to collect counts from 111In-labeled platelets. Thrombi established 30 min after injury, otherwise stable for 6 h, clear during 30-60 min of continuous infusion of either hirudin, tick anticoagulant or activated porcine protein C, or intermittent activation of endogenous protein C with a latent thrombin reagent. Anticoagulant dose-dependence of thrombus clearance is established for hirudin between 0.01 and 1.0 mg/kg/min. Thrombi become progressively refractory to hirudin between 0.5 and 6 h after injury. Neither heparin nor low-molecular-weight heparin in full (clinical) anticoagulant doses yield significant dethrombosis. It is concluded that, within time limits, controlled thrombin generation in platelet thrombi maintains platelet cohesion without catalyzing irreversible platelet aggregation or clotting of fibrinogen.
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Sunardi, Agus, Nadjwa Zamalek Dalimoenthe, Coriejati Rita, and Adhi Kristianto Sugianli. "THE CORRELATION BETWEEN THE MEAN PLATELET VOLUME VALUES WITH THROMBOCYTE AGGREGATION IN NEPHROPATHY DIABETIC PATIENTS." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 25, no. 1 (April 10, 2019): 79. http://dx.doi.org/10.24293/ijcpml.v25i1.1510.
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Diabetic nephropathy is the most important cause of end-stage renal failure. Chronic hyperglycemia will cause glomerular endothelial damage, and this damage will stimulate hemostasis activation including platelets so that platelet aggregation will increase. The increase of platelet aggregation will increase platelet consumption, which further stimulates thrombopoiesis which will lead to immature platelets of large size to be released into the circulation. This research aimed to determine the positive correlation between MPV with platelet aggregation in patients with diabetic nephropathy. This study was an analytic observational study with a cross-sectional study design. The research was conducted in the Dr. Hasan Sadikin Hospital Bandung from July 2016 to October 2017. A total of 52 subjects who met the inclusion criteria were included in the study. Mean platelet volume and platelet aggregation were performed with venous examination with EDTA and sodium citrate 3.2% anticoagulants. The result of platelet aggregation examination showing platelet hyper-aggregation was found in 44.2% of subjects, 50% normal-aggregation, 5.8% hypo-aggregation. While the median value of MPV in this study was 9.2 fL with the range of 8.00 – 11.80 fL. A positive correlation was found between MPV value with platelet aggregation with r= 0.067, p= 0.634. The conclusion was that there was no correlation between MPV values with platelet aggregation in diabetic nephropathy patients. This small and insignificant r-value might be due to several factors that also affect platelet aggregation in diabetic nephropathy patients, requiring further investigation.
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Eslam, Roza Badr, Nina Reiter, Alexandra Kaider, Irene Lang, and Simon Panzer. "High-shear- and-thrombin-inducible platelet adhesion and aggregation in patients undergoing percutaneous coronary intervention." Thrombosis and Haemostasis 105, no. 03 (2011): 496–500. http://dx.doi.org/10.1160/th10-06-0384.
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SummaryThrombin-generation and activation of platelets during percutaneous coronary intervention (PCI) play a key role for early thrombotic events. Heparin and bivalirudin are approved anticoagulants for PCI. We examined the specific effects of these anticoagulants on platelet adhesion and aggregation under high shear conditions, and the presence of excess thrombin. To simulate in vivo conditions that may precipitate a bleeding/thrombotic event, we added thrombin in vitro to blood samples from 89 stable patients who had been randomly assigned to receive heparin or bivalirudin for elective PCI and examined thrombininducible platelet adhesion and aggregation under high shear conditions. Platelet adhesion increased by 10% of baseline with heparin, but decreased by 20% with bivalirudin (p=0.0047). Thrombin-inducible platelet adhesion and size of aggregates was equally inhibited by heparin and bivalirudin. Thus, under high shear conditions and excessive thrombin generation as they occur in atherosclerotic vascular compartments and acute vascular syndromes, heparin and bivalirudin inhibit thrombin-induced platelet adhesion and aggregation to a similar extent, while they have opposite effects on platelet adhesion in the absence of thrombin.This study was part of the doctorial thesis of NR at the Department of Blood Group Serology and Transfusion Medicine.
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Fareed, Jawed, Debra Hoppensteadt, Omer Iqbal, Josephine Cunanan, Vinod Bansal, Schuharazad Abro, and Rakesh Wahi. "Defibrotide Interactions with Newer Oral Anticoagulants and Antithrombotic Agents." Blood 120, no. 21 (November 16, 2012): 3411. http://dx.doi.org/10.1182/blood.v120.21.3411.3411.
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Abstract Abstract 3411 Defibrotide is a polydisperse mixture of porcine-derived single-stranded oligonucleotides which has been used for multiple clinical indications. Recent clinical trials of defibrotide indicate that this drug may provide benefits both for the treatment and prophylaxis of hepatic veno-occlusive disease (VOD) in hematopoietic stem cell therapy. In VOD it is believed that defibrotide exerts two distinct effects; 1. Endothelial cell protection and 2. Restoration of the thrombotic-fibrinolytic balance. Although antithrombotic in nature, defibrotide does not produce any systemic anticoagulant effects atthe selected dose of 25 mg/kg/day Conventional oral anticoagulants are routinely not used in veno-occlusive disease however heparin is often used in the management of these patients. More recently, newer oral anticoagulant drugs such as dabigatran, apixiban and rivaroxiban have been approved for the management of post orthopaedic surgical venous thrombosis and stroke prevention in atrial fibrillation. The current study was undertaken to investigate the effect of defibrotide on the anticoagulant and antiprotease effects of the newer oral anticoagulant drugs in the whole blood, plasma and platelet rich plasma based systems. Materials and Methods Native whole blood was drawn from 25 normal healthy individuals and supplemented with 100 μg/mL defibrotide and 250 ng/mL of each of the individual oral anticoagulant drugs alone and with defibrotide. Activated clotting time (ACT) measurements were made on a Hemachron instrument using celite ACT tubes. For the plasma based anticoagulant studies, a fixed concentration of defibrotide of 100 μg/mL was supplemented with defibrotide to pool plasma alone and with each of the individual oral anticoagulantagents in a concentration range of 0–1000 ng/mL. To investigate the effect of defibrotide on agonist induced platelet aggregation platelet rich plasma was prepared with varying amounts of defibrotide (0–100ug/ml). Such agonsits as ADP, epinephrine, collagen and arachodonic acid were used. To test the effects of newer oral anticoagulants, each agent was supplemented at 250–500ng/ml to the defibrotide enriched PRP (100ug/ml) and agonist induced aggregation studies were carried out in comparison to saline and defibrotide control. To test the effect of defibrotide on the conventional oral anticoagulant agents, plasma samples from patients with INR range of 1.5–3.0 were supplemented with 100ug/ml and the PT/INR was re-determined using Innovin® reagent. Results In the whole blood studies apixaban and rivaroxaban did not produce any prolongation of the whole blood ACT. However, dabigatran produced a modest increase in the ACT at 250 ng/mL. In the anticoagulant assays, supplementation of these agents did not result in any prolongation of the PT with defibrotide and newer oral anticoagulants. In the aPTT assay, the apixaban and rivaroxaban did not have any interaction, at a concentration greater than 500 ng/mL. Dabigatran shows a slight interaction in the aPTT assay. Defibrotide, did not produce any alterations of the effect on the agonist (ADP, epinephrine, collagen, arachidonic acid) induced aggregation of platelets in concentrations up to 100 μg/mL. Studies carried out where defibrotide at 100 μg/mL is combined with 250 ng/mL of each of the new anticoagulants does not show any modification of the aggregation responses. Defibrotide supplementation to anti-platelet therapy treated patient's blood collected did not result in any augmentation of the observed inhibitory responses. Defibrotide did not produce any changes in the PT/INR values of plasma samples collected from warfarin treated patients at concentrations of up to 100 μg/ml. Conclusions These studies indicate that in a concentration range of 0–1000 ng/mL the new anticoagulants do not exhibit any significant interactions with defibrotide. Since dabigatran exhibits some anticoagulant effect of its own, minor interactions with defibrotide may be observed. Based on the indications for the new oral anticoagulant drugs, their circulating levels and rapid clearance, it is unlikely that defibrotide will produce any interactions with these drugs. Disclosures: No relevant conflicts of interest to declare.
Dissertations / Theses on the topic "Anticoagulants Platelet Aggregation"
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Fornari, Luciana Savoy. ""Fibrilação atrial e tratamento antitrombótico em pacientes atendidos em hospital especializado em cardiologia no Brasil"." Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-13042006-120958/.
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Objetivo: Avaliar o uso de antitrombóticos em pacientes com fibrilação atrial (FA) em hospital cardiológico no Brasil (InCor).Métodos e resultados: Um estudo observacional transversal analisou os prontuários de todos os pacientes atendidos no InCor em cada um de 5 dias separados no ano de 2002 (Fase 1), sendo prospectivamente reanalisados após 1 ano (Fase 2). A prevalência da FA nos 3764 prontuários analisados foi de 8%. Antiplaquetários foram prescritos para 21,26% e 19,93%, anticoagulantes para 46,51% e 57,81%, e 32,23% e 22,26% não usavam nenhum antitrombótico nas Fases 1 e 2, respectivamente. Somente 15,60% e 23,25% apresentavam níveis de RNI terapêuticos.Conclusão: A anticoagulação é subutilizada nos pacientes com FA apesar do fato de serem tratados por cardiologistas em um hospital universitárioObjective: To assess antithrombotic therapy among atrial fibrillation (AF) patients in a Brazilian University Heart Hospital (InCor).Methods and results: A cross sectional study analyzed the charts of all patients treated at InCor in 5 separate days of 2002 (Phase 1), and prospectively reviewed them after one year (Phase 2). The prevalence of AF in the 3,764 assessed charts was of 8.0%. Antiplatelets were prescribed to 21.26% and 19.93%, anticoagulants to 46.51% and 57.81%, and 32.23% and 22.26% were not receiving any antithrombotic in Phases 1 and 2, respectively. Only 15.60% and 23.25% were within INR therapeutic range.Conclusion: Anticoagulation is underused in AF patients besides the fact of being treated by cardiologists in a University Hospital
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Granat, Fanny. "Agrégation plaquettaire in vitro : effets anticoagulants du CTAD et utilisation à des fins diagnostiques dans les espèces sensibles." Thesis, Toulouse, INPT, 2016. http://www.theses.fr/2016INPT0029/document.
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La numération plaquettaire est une analyse délicate et le résultat est souvent erroné notamment du fait d’une tendance à l’agrégation in vitro dans certaines espèces animales. Il a ainsi pu être démontré chez le Chat que ce phénomène peut être inhibé par l’association d’un anticoagulant avec des inhibiteurs plaquettaires : le CTAD (Citrate, Théophylline, Adénosine et Dipyridamole). Cette association permet ainsi l’obtention de numérations plaquettaires fiables sans affecter les autres populations sanguines, mais également d’effectuer des analyses d’hémostase et de biochimie. De nouveaux intervalles de référence ont dû être établis pour certaines variables hématologiques avec les analyseurs utilisés en laboratoire et dans les cliniques vétérinaires. Par ailleurs, si les effets antiagrégants du CTAD sont moins nets chez le Chien, il peut également servir d’anticoagulant « universel », permettant de réduire le nombre de prélèvements et d’améliorer ainsi le bien-être des animauxThe platelet count is a delicate measurement, which may often be erroneous because of the tendency of platelets from some animal species to aggregate in vitro. This study demonstrated that this effect can be inhibited in cats using CTAD (Citrate, Theophylline, Adenosine and Dipyridamole) composed of an anticoagulant and platelet inhibitors. This association provides reliable platelet counts without affecting other blood populations and also allows hemostasis and biochemical analyses. New hematological reference intervals have been established for some variables with analyzers used in clinical pathology laboratories and veterinary clinics. Furthermore, if the antiplatelet clumping effects of CTAD are less marked in canine species, the CTAD can also serve as "universal" anticoagulant, reducing the number of blood samples and thus improving animal welfare
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PierdonÃ, Taiana MagalhÃes. "AvaliaÃÃo das atividades antiagregante plaquetÃria e anticoagulante em estudo de bioprospecÃÃo de Opercutina macrocarpa (L.) Urb. (Jalapa) em plasma humano: determinaÃÃo do mecanismo de aÃÃo." Universidade Federal do CearÃ, 2011. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=9287.
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Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgicoOperculina macrocarpa (L.) Urb. (âjalapa brasileiraâ) (Convolvulaceae) à uma espÃcie comum do Nordeste brasileiro, sendo popularmente utilizada pelas suas propriedades laxativa, purgativa e âdepurativaâ. A tintura do tubÃrculo de jalapa, matÃria-prima majoritÃria, ao lado da tintura de Convolvulus scammonia (TCS) compÃem o fitoterÃpico Aguardente Alemà(AAL) ou Tintura de Jalapa Composta, indicada como antitrombÃtico na medicina popular. O objetivo do presente trabalho foi investigar o potencial antiagregante plaquetÃrio e anticoagulante de O. macrocarpa em plasma humano, incluindo estudo de bioprospecÃÃo e determinaÃÃo do possÃvel mecanismo de aÃÃo. A avaliaÃÃo da atividade antiagregante plaquetÃria das drogas testes (tintura e fraÃÃes de O. macrocarpa, TCS e AAL) em plasma humano rico em plaquetas (PRP) foi mensurada por mÃtodo turbidimÃtrico, sendo a agregaÃÃo induzida por vÃrios agonistas como difosfato de adenosina (ADP), epinefrina (EPI), Ãcido araquidÃnico (AA), colÃgeno (COL) ou trombina (TROM). Ao contrÃrio da TCS e da AAL, tanto a tintura de O. macrocarpa (TOM/precipitado(P) e sobrenadante(S)) quanto uma das fraÃÃes orgÃnicas obtidas da planta (TOM/1-F4) mostraram atividade antiagregante plaquetÃria, onde a TOM/1-F4 (100 Âg/mL) apresentou efeito comparÃvel ao Ãcido acetilsalicÃlico (AAS). CaracterizaÃÃo fÃsico-quÃmica (CLAE e espectrofotometria) da TOM/PS (teor de resinas 1,38g%) e da TOM/1-F4 permitiu a identificaÃÃo de Ãcidos fenÃlicos (clorogÃnico, gÃlico e cafÃico), bem como a determinaÃÃo do teor de fenÃis totais da TOM (0,14g%). O efeito antiagregante plaquetÃrio da TOM/PS e da TOM/1F-4 parece resultar de vÃrias aÃÃes intracelulares. Contudo, a TOM/PS na presenÃa do AAS, L-ARG, ODQ, pentoxifilina (PTX) ou ticlopidina (TIC) teve seu efeito antiagregante plaquetÃrio modificado principalmente pela TIC, sugerindo um papel importante dos receptores purinÃrgicos na bioatividade da TOM/PS. A TOM/PS apresentou atividade antioxidante determinada atravÃs do teste do DPPH. AlÃm disso, a TOM/PS e a TOM/1F-4 nÃo mostraram aÃÃo anticoagulante em plasma humano, mas a TOM/PS aumentou o tempo de sangramento em camundongos. Foi observada uma toxicidade relativa da TOM/PS em neutrÃfilo humano. Dessa forma, o presente estudo comprovou, de maneira inÃdita, o potencial antiagregante plaquetÃrio da tintura e da fraÃÃo orgÃnica de jalapa, que estÃo pelo menos em parte relacionados à presenÃa de fenÃis, particularmente Ãcidos fenÃlicos, e resinas na planta.
Operculina macrocarpa (L.) Urb ("Brazilian jalapa") (Convolvulaceae) is a common species of the Brazilian Northeast. It is popularly used because of its laxative and purgative properties. The tincture of Operculina macrocarpa tubers (major constituent) and Convolvulus scammonia composes the raw materials of Aguardente AlemÃÂ, herbal medicine, referred to as antithrombotic in folk medicine. The objective of this study was to investigate the antiplatelet and anticoagulant potential for Operculina macrocarpa in human plasma, including the bioprospection study and determination of possible mechanism of action. The evaluation of antiplatelet activity of drugs (tincture and fractions of O. macrocarpa, tincture of C. scammonia and AAL) in human platelet-rich plasma (PRP) was measured by the turbidimetric method where the aggregation was induced by the addition of agonists (adenosine diphosphate (ADP), epinephrine (EPI), arachidonic acid (AA) collagen (COL) or thrombin (TROM). Unlike tincture of C. scammonia and AAL, both O. macrocarpa tincture (TOM/preciptade (P) and supernatant (S)) and one of the organic fractions obtained from O. macrocarpa (TOM/1-F4) showed antiplatelet activity in human plasma where TOM/1-F4 (100 Âg/mL) presented comparable effect to AAS. Physicochemical characterization (HPLC and spectrophotometer) of TOM/PS (content of resins 1,38g%) and TOM/1-F4 allowed the identification of phenolic acids (chlorogenic, galic and caffeic) as well as the determination of total phenols of TOM (0,14g%). The antiplatelet effect of TOM/PS and TOM/1-F4 seems to result from many intracellular actions. However, TOM/PS in presence of AAS, L-ARG, ODQ, pentoxifilin (PTX) or ticlopidine (TIC) had its antiplatelet effect modified mainly because of TIC, suggesting an important role of purinergic receptors in TOM/PS. TOM/PS presented antioxidant activity determined by DPPH test. Furthermore, TOM/PS and TOM/1-F4 did not showed anticoagulant action in human plasma but TOM/PS increased the bleeding time in mice. It was observed a relative toxicity of TOM/PS in human neutrophil. Therefore, this study demonstrated, as never before, the antiplatelet potencial of tincture and the organic fraction of "jalapa" and that at least related to the presence of phenols, particulary phenolic acids, and resins in plant.
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Arantes, Flávia Bittar Britto. "Efeito dos anticoagulantes sobre a agregabilidade plaquetária: ação da heparina de baixo peso molecular enoxaparina, e do inibidor direto da trombina dabigatrana." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-22102018-135800/.
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Introdução: A interação entre os anticoagulantes e a agregabilidade plaquetária é complexa. Dados laboratoriais prévios mostraram que a dabigatrana aumenta a excreção urinária de metabólito do tromboxano, indicando efeito de ativação de plaquetas. Posteriormente, dados do estudo RELY sugeriram que a dabigatrana 150mg poderia aumentar o risco de infarto do miocárdio em pacientes com fibrilação atrial. Objetivos: Comparar a influência da Dabigatrana e Enoxaparina na agregabilidade plaquetária. Métodos: Estudo prospectivo, intervencionista, realizado em pacientes com doença arterial coronariana (DAC) crônica em uso de aspirina em baixas doses. Os indivíduos foram inicialmente designados para dabigatrana 150mg, 2x/dia, por 5 dias, seguido por um período de washout de 30 dias e depois para exoxaparina 1mg/kg, 2x/dia, por um período adicional de 5 dias. Os testes de função plaquetária foram realizados no início e após cada fase de intervenção, usando agregometria de sangue total p (MEA) (objetivo primário), ELISA para determinação quantitativa de tromboxano B2 (TXB2), Verify Now Aspirin e testes de coagulação (objetivos secundários). Resultados: Em comparação com os valores basais, a dabigatrana aumentou a agregabilidade plaquetária avaliada pelo teste MEA-ASPI (+5U ± 24,1), enquanto a enoxaparina diminuiu a agregabilidade plaquetária (-6U ± 22,2), p=0,012 para a comparação entre os grupos ). O mesmo padrão foi observado usando o ensaio TXB2 (+2pg/mL para dabigatrana, -13pg/mL para enoxaparina, p = 0,011). Não houve diferenças significativas entre os dois grupos em relação aos demais testes. Individualmente, a enoxaparina diminuiu significativamente a agregabilidade plaquetária por TXB2 [33 (16,5 - 95)pg/mL vs. 20 (10-52) pg/mL, respectivamente, p = 0,026), mas não foram observadas diferenças significativas individuais com a dabigatrana em relação aos valores basais. Conclusões: Em relação à agregabilidade plaquetária, há um efeito oposto significativo da dabigatrana (aumento) em comparação com a enoxaparina (diminuição). Individualmente, foi observada uma diminuição significativa na agregabilidade plaquetária apenas com a enoxaparina, quando comparada com valores basaisBackground: The interaction between anticoagulants and platelet aggregation is complex. Previous laboratory data have shown that dabigatran increases urinary thromboxane metabolite excretion, indicating platelet-activating effect. Thereafter, data from RELY trial suggested that dabigatran 150mg could enhance the risk of myocardial infarction in atrial fibrillation patients. Objectives: To compare the influence of Dabigatran and Enoxaparin on platelet aggregation. Methods: Prospective, interventional study conducted in chronic coronary artery disease (CAD) patients taking low-dose aspirin. Subjects were assigned initially to dabigatran 150mg bid for 5 days followed by a washout period of 30 days and then to exoxaparin 1mg/kg bid for an additional 5 days period. Platelet function tests were performed at baseline and after each intervention phase using multiple electrode aggregometry (MEA) (primary endpoint), ELISA for plasma quantitative determination of thromboxane B2, Verify Now Aspirin and coagulation tests as secondary endpoints. Results: In comparison with the baseline values, dabigatran increased platelet aggregation evaluated by MEAASPI test (+5U ± 24.1), whereas enoxaparin decreased platelet aggregation (- 6U± 22.2), p=0.012 for the comparison between the groups). The same pattern was observed using theTxB2 assay (+2pg/mL for dabigatran, -13pg/mL for enoxaparin, p=0.011). There were no significant differences between both groups regarding the VerifyNow Aspirin or the other platelet function and coagulation tests utilized. Individually, enoxaparin significantly decreased platelet aggregation by TXB2 [33 (16,5 - 95) pg/mL vs. 20 (10-52) pg/mL, respectivamente, p = 0.026) but no significant differences were observed with dabigatran when individually compared to baseline. Conclusions: Regarding platelet aggregation, there is a significant opposite effect of dabigatran (increase) in comparison with enoxaparin (decrease). Individually, a significant decrease in platelet aggrebability was observed with enoxaparin, but no significant differences were observed with dabigatran
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Azevedo, Tarciana Carvalho Gurgel de. "A??o de polissacar?deos sulfatados de Fucus Vesiculosus na Hemostasia e no sistema complemento." Universidade Federal do Rio Grande do Norte, 2006. http://repositorio.ufrn.br:8080/jspui/handle/123456789/12606.
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Fucans are a family of sulfated homo and teropolysaccharides respectively, composed mainly of a- (1?2) and a- (1?3) linked by L-fucose residues. Properties such as the ability to act as an anti-contraceptive, to reduce cholesterol levels, and to act as an anti-tumor agent are much related. We have focused our attention on the anticoagulant properties, platelet aggregation, hemorrhagic activity and complement system in vitro of commercial fucoidan (F) and their purified fractions (F1, F2 and F3) from Fucus vesiculosus obtained from fractionation of the fucoidan with different concentrations of acetone 1, 2 and 3v. These compounds were chemically characterized and the fucoidan (F) was modified by desulfation. The anticoagulant activity of the compounds was assessment by activated partial thromboplastin time (APTT) and prothrombine time assay (PT) using citrated normal human plasma. The results of APPT test showed that F, F1 and F2 have high anticoagulants activities 240.0 s (5 ?g). The F3 showed 73.7 s in the same concentrations. The results obtained with PT test to F, F1, F2 and F3 were 81.5 s, 120.0 s, 57.1 and 32.5 s respectively with 50 ?g. The dessulfated polymer showed a decrease in the anticoagulant activity in these two tests. Platelet aggregation assay was measured turbidimetrically with platelet aggregometer by method of Born. The aggregation platelet with F and fractions F1, F2 and F3 exhibited a two-phase answer in the concentration of 5 mg/mL with maximum aggregation of 76.36 ? 10.3% ; 69.54 ? 9.40%; 75.94 ? 9.01%; 51.13 ? 9.59% respectively. However, was observed a hipoaggregate profile F (15.17 ? 5.2%), F1 (7.40 ? 3.04 %), F2 (19.1 ? 5.41%) and F3 (5.09 ? 3.02%) at 0.1 mg/mL. The hemorrhagic activity assay was carried in Wistar rats and showed that these compounds have low hemorrhagic effect when compared to heparin. The complement system ( alternative pathway was made using non-sensibilized rabbit red blood cells The results of complement system essay showed that F , F2 and F3 have action inhibitory in relation to the group control 0.544, 0.697, 0.622 and 0.958 respectively The results showed that these compounds have action on this system. Interaction of the polisaccharides with proteins C3 and C4 showed that the fraction F1 stimulated the activity assay hemolytic using red blood cells
Fucanas s?o uma fam?lia de homo e hetero polissacar?deos sulfatados, formadas por uma cadeia central com liga??es α-(1→2) ou α-(1→3) unidas atrav?s de res?duos de L-fucose. Propriedades como a habilidade para agir como um anticoncepcional, reduzir n?veis de colesterol, e agir como um agente anti-tumoral foram relatadas. N?s focalizamos nossa aten??o nas propriedades anticoagulantes, agrega??o plaquet?ria, atividade anti-hemost?tica e sistema de complemento in vitro do fucoidan comercial e das fra??es F1, F2 e F3 de Fucus vesiculosus obtidas atrav?s do fracionamento do fucoidan por precipta??o com acetona (1, 2 e 3v). A atividade anticoagulante dos compostos foi avaliada pelo tempo de tromboplastina parcial ativado (APTT) e o tempo de protrombina (PT) usando plasma humano citratado. Os resultados do teste de APPT mostraram que o Fucoidan (F) e as fra??es F1 e F2 t?m altas atividades anticoagulantes 240,0 s (5 ?g), enquanto que a F3 mostrou 73,7s nas mesma concentra??o. Os resultados obtidos com PT para o F, F1, F2 e F3 foram 81,5 s, 120,0 s, 57,1 e 32,5 s respectivamente usando a massa de 50 ?g. A dessulfata??o do Fucoidan demonstrou uma diminui??o da atividade anticoagulante nos dois testes. O ensaio de agrega??o plaquet?ria foi realizado no agregometro de acordo com o m?todo de Born. A agrega??o plaquet?ria induzida pelo fucoidam e pelas fra??es de F1, F2 e F3 exibiram uma resposta bif?sica na concentra??o de 5 mg/mL com amplitude m?xima de agrega??o de 76,36% ? 10,3%; 69,54% ? 9,40%; 75,94% ? 9,01%; 51,13% ? 9,59% respectivamente. Por?m, na concentra??o 0,1 mg/mL foi observada um perfil hipoagregante para o Fucoidan (15,17% ? 5,2) e para as fra??es F1 (7,4% ? 3,04%), F2 (19,1% ? 5,41) e F3 (5,09% ? 3,02%). A atividade anti-hemost?tica foi realizada com ratos machos da linhagem Wistar e demonstrou que estes compostos t?m efeito hemorr?gico residual menor do que o da heparina. A a??o dos polissacar?deos fucosilados sulfatados na via alternativa do sistema complemento foi realizada atrav?s da utiliza??o de eritr?citos de coelhos n?o sensibilizados. Os resultados para o Sistema Complemento mostraram que o F, F2 e F3 t?m a??o neste sistema, apresentando efeito inibit?rio em rela??o ao grupo controle 0,544, 0,697, 0,622 e 0,958 respectivamente. Intera??es dos polissacar?deos com as prote?nas C3 e C4 demonstraram que a fra??o F1 estimula a atividade hemol?tica do complemento usando eritr?citos de coelho. Conclu?mos que estes a??cares t?m atividade anticoagulante e atuam como inibidores do sistema complemento sendo uma valiosa droga que pode ser empregada em doen?as relacionadas com inflama??o e coagula??o sang??nea
Books on the topic "Anticoagulants Platelet Aggregation"
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Anticoagulants, antiplatelets, and thrombolytics. 2nd ed. New York, NY: Humana, 2010.
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Handbook of compounds with anti-inflammatory and anti-platelet aggregation activities isolated from plants. New York: Nova Science Publishers, 2008.
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Waksman, Ron, and Andrew E. Ajani. Pharmacology in the catheterization laboratory. Chichester, West Sussex, UK: Wiley-Blackwell, 2009.
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Dwyer, Scott Douglas. Effects of anesthetics, anticoagulants, and rat strain on rat platelet aggregation. 1985.
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A, Mousa Shaker, ed. Anticoagulants, antiplatelets, and thrombolytics. Totowa, N.J: Humana Press, 2004.
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A, Mousa Shaker, ed. Anticoagulants, antiplatelets, and thrombolytics. Totowa, N.J: Humana Press, 2004.
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Mousa, Shaker A. Anticoagulants, Antiplatelets, and Thrombolytics (Methods in Molecular Medicine). Humana Press, 2003.
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Ron, Waksman, and Ajani Andrew A. E, eds. Pharmacology in the catheterization laboratory. Chichester, West Sussex, UK: Wiley-Blackwell, 2009.
Find full textBook chapters on the topic "Anticoagulants Platelet Aggregation"
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Köstenberger, M., S. Gallistl, G. Cvirn, M. Petritsch, B. Leschnik, and W. Muntean. "In vitro Effects of combined Administration of Eptifibatide and Anticoagulants on Thrombin induced Platelet Aggregation after high versus low Coagulant Activation of Platelet Rich Plasma." In 32nd Hemophilia Symposium Hamburg 2001, 247–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-18150-4_40.
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Köstenberger, M., S. Gallistl, G. Cvirn, B. Roschitz, and W. Muntean. "Glycoprotein IIb/IIIa Receptor Antagonist c7E3 Fab and Anticoagulants Show an Additive Effect on Thrombin-Induced Platelet Aggregation after High Coagulant Challenge in Vitro." In 30th Hemophilia Symposium Hamburg 1999, 369–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-18240-2_58.
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Thompson, Carrie A. "Malignant Hematologic Disorders." In Mayo Clinic Internal Medicine Board Review, 427–38. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190464868.003.0039.
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The 2 essential functions of the coagulation system (maintaining hemostasis and preventing and limiting thrombosis) are served by the procoagulant and anticoagulant components. Vascular injury results in activation of the phases of hemostasis, including vasospasm, platelet plug formation (platelet activation, adhesion, and aggregation), and fibrin clot formation (by activation of coagulation factors in the procoagulant system). The anticoagulant system controls excessive clot formation, while the fibrinolytic system breaks down and remodels blood clots.
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Kubisz, Peter, Pavol Holly, and Jan Stasko. "Bleeding in Patients with Antiphospholipid Antibodies." In Antiphospholipid Syndrome - Recent Advances in Basic and Clinical Aspects [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97856.
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The antiphospholipid antibodies (aPL) are commonly associated with thrombotic events and obstetric complications. However, apart from the bleeding complications of antithrombotic therapy, the acquired coagulopathy caused by the aPL, particularly by lupus anticoagulant and anticardiolipin antibodies, might be occasionally manifested as a hemorrhagic syndrome with various clinical severity. Bleeding symptoms vary from mild (mucocutaneous) up to life-threatening (gastrointestinal, intracranial). The bleeding may be the first manifestation of aPL or appear concomitantly with thrombosis. The underlying hemostatic changes include thrombocytopenia, platelet function disorders, and coagulation factor inhibitors or deficiencies, namely prothrombin, FVII, FVIII, FX, and FXI. Thrombocytopenia is the most common finding, seen in up to 53% of patients with aPL, although it is usually mild to moderate and associated with significant bleeding only in a minority of cases. Of interest, patients with severe thrombocytopenia appear to be less likely to suffer from thrombotic events. The involved pathophysiological mechanisms are heterogeneous. Non-neutralizing antibodies against coagulation factors resulting in increased clearance, specific antibodies against platelet membrane glycoproteins, increasing platelet activation and aggregation with subsequent consumption, and immune-mediated platelet clearance are among those identified. Immunosuppression, preferably with corticosteroids, represents the first-choice therapeutic approach. Plasmapheresis is efficient in the case of catastrophic antiphospholipid syndrome. Antithrombotic therapy can be challenging, but its administration should continue as much as possible.
Conference papers on the topic "Anticoagulants Platelet Aggregation"
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Corte-lazzo, D., M. Galli, P. Viero, and T. Barbui. "INTERACTION BETWEEN LUPUS ANTICOAGULANT AND PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644230.
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Lupus Anticoagulants (LAC) are IgG or IgM immunoglobulins which interfere with phospholipid-dependent coagulation tests and actively react also with platelet wall phospholipids. This interaction may result in platelet quantitative and qualitative defects. We have examined 10 patients with LAC diagnosed on the basis of the commonly accepted criteria (Working Party reccomandations, 1983). Four had concomitant Systemis Lupus Erythematosus, one Waldenstrom's disease (W. D.) and five no apparently underlying disease. Only the case with W. D. presented bleeding tendency, whereas the others had a history of thrombotic complications. A vei?y striking defect of platelet aggregation by ADP, epinephrine, collagen and arachidonic acid was documented in the case of W. D., who had also a very prolonged bleeding time (>20 minutes) ; ,in this latter case LAC was an IgM. In the others, LAC, identified as IgG immunoglobulins, produced no aggregation abnormalities. On the contrary, serotonin platelet concentration, platelet, plasma and urine Beta-Thromboglobulin contents showed values consistent with a pattern of platelet activation in all cases. IgG immunoglobulins separated from sera of six patients showed LAC activity but no effects on platelet aggregation of a normal PRP, whereas induced secretion of Beta-Thromboglobulin from normal platelets.
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Saba, S. R., H. I. Saba, and G. A. Morelli. "EFFECT OF COLLAGEN AND CITRATE ON HEPARIN-HEDIATED PLATELET ANTIAGGREGATORY ACTIVITY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642869.
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Heparin has been reported to inhibit platelet aggregation. Our studies show that this activity is easily demonstrable in washed platelet systems, but fails to occur in citrated platelet-rich plasma (PRP) in the presence of a variety of agonists, except collagen. Studies were performed to answer the following questions: (1) Why does heparin inhibit the aggregation of washed platelets but not of citrated PRP, which is the system commonly used for platelet aggregation studies? (2) What is the effect of heparin on platelet aggregation occurring in whole blood, where it can be examined both with and without the presence of sodium citrate? (3) Why does heparin consistently inhibit the collagen-induced aggregation even in citrated PRP, while it fails to inhibit aggregation caused by other agonists? Results of the studies clearly demonstrated that heparin has the ability to directly react with sodium citrate, causing loss of its inhibitory activity on platelets. The antiaggregatory activity of heparin in the presence of collagen as the agonists appears to be directly related to the blocking of collagen’s agonist activity by heparin. Small concentrations of heparin which were unable to inhibit aggregation per se, effectively blocked the collagen agonist activity on platelet aggregation when heparin was directly added to collagen. Further studies showed that heparin, in a native whole blood platelet aggregation system (in the absence of any anticoagulant), exhibited significant inhibitory activity. This activity was lost when citrate was present in the whole blood preparation. These studies, therefore, indicate that failure of heparin to inhibit platelet aggregation in citrated PRP does not negate the importance of this inhibitory activity. Reactivity of heparin with sodium citrate renders citrated systems unsuitable for studying heparin's effect upon platelets. The whole blood platelet aggregation system without the presence of anticoagulants appears to be a more suitable system for the study of heparin and platelet aggregation, and is closer to the physiological system. Heparin exhibits marked inhibitory activity on platelet aggregation in this system, and this suggests it may be an important activity which deserves further attention.
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Bagdy, D., É. Bara-bás, L. Sebestyén, M. Diószegi, Zs Fittler, S. Bajusz, and E. Széll. "CORRELATION BETWEEN THE ANTICOAGULANT AND ANTIPLATELET EFFECT OF D-PHE-PRO-ARG-H (RG-2958)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643448.
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Anticoagulants usually have no antiplatelet effect and platelet function inhibitors do not interact with the coagulation factors. Since thrombin has a decisive role in thrombus formation (growth and stabilization), inhibitors of the effect of thrombin on platelets may be of special importance in developing a novel type of anticoagulant with antiplatelet properties.D-Phe-Pro-Arg-H /I/ designed and synthetized in our Institute was found to be a highly specific,reversible non-competitive inhibitorgOf thrombin,a specific platelet agonist. (K.= 1x10-8 M). /I/ was administered parenterally and orally to white New Zealand rabbits and to beagle dogs. The kinetics of action was recorded by measuring the WBCT, APTT, PT, TT,platelet count (PC) and platelet aggregation (PA). Optimum degree of anticoagulation was considered by the values proposed by Verstraete and Verwilghen. /I/ was shown to be a highly specific inhibitor of PA induced by thrombin.No direct interaction between the inhibitor and the platelet membrane could be detected. Aggregability of human platelets in citrated PRP and that of the gel-filtrated platelets induced by ADP or collagen did not change after incubation with /I/. The antiplatelet effect of /I/ was studied by ex vivo experiments where the inhibitor was the anticoagulant ( 30 ug/ml whole blood ) instead of citrate. Comparing the aggregability caused by several inducers in citrated human PRP with that of in /I/-PRP a significant difference was observed when epinephrine was the PA-inducer. /I/ acts via formation of an enzyme-inhibitor complex that inhibits the binding of thrombin on their receptor-sites at the platelet membrane. In vivo experiments showed a close correlation between TT and PA induced by thrombin. /I/ proved completely harmless to platelets and red blood cells. No significant change in PC could be detected.
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Gool, R. Van, C. P. M. Reutelingsperger, G. Hornstra, and H. C. Hemkera. "PLATELET FUNCTION IN PLASMA AT PHYSIOLOGICAL CALCIUM CONCENTRATION. THE USE OF VAC AS AN ANTICOAGULANT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643764.
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We have purified from human placenta an anticoagulatory protein (VAC, Mr= 32,000), which inhibits phospholipid dependent procoagulant reactions through a calcium dependent high affinity binding to procoagulant phospholipids..When tested in citrated platelet rich plasma (cPRP), VAC does not affect platelet aggregation and secretion in reponse to ADP, collagen and thrombin. Purified VAC (0.05 μM, final concentration; f.c.) was used as an anticoagulant to prepare PRP (VAC-PRP). Platelet aggregation (optical density method) and release of newly absorbed 14C-sero-tonin (5HT) in response to adenosine diphospate (ADP) were measured and compared with platelet responses incPRP obtained simultaneously fromthe same donor.The response of ADP stimulated platelets in VAC-PRP differs strikingly from that in cPRP. In the latter, platelets react with a dose-dependent primary aggregation, followed by a thrombin (Ila)-independent second wave of aggregation associated with 5HT-secre-tion.Platelets in VAC-PRP, however, demonstratean increased primary aggregation in responseto ADP, which is followed by a IIa-mediated second wave of aggregation and 5HT-secretion.Increasing the VAC concentration does not affect the primary aggregation response, but delayed the IIa-dependent secondary events in a dose-dependent way. At 0.5 μ M VAC, platelets react to ADP (10 μM f.c.) with reversible aggregation only. No matter this high ADP-dose, secretion reaction does not occur. At this VAC concentration, epinephrine (5 μM f.c.) does not cause aggregation and 5HT-release at all, whereas incPRP both reactions occur quite readily. Although in VAC-PRP, epinephrine retains its synergistic effect on ADP to aggregate platelets, no 5HT release was ever observed and the resulting aggregation was alwaysreversible It is concluded that VAC is a suitable anticoagulant to investigate platelet function in the presence of physiological calcium concentration. Since platelet aggregation and release appear very different from results obtained in the usual way (cPRP, low calcium concentration) the physiological meaning of this latter method needs re-evaluation. Finally, our results cast severe doubt on epinephrine as an important platelet stimulant under physiological conditions.
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Heptner, W., J. R. Suárez, and V. Lütgendorf. "STUDIES ON PLATELET AGGREGATION BY IMPEDANCE AGGREGOMETRY AND ATP SECRETION IN NON-ANTICOAGULANT BLOOD." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644810.
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Investigations in vitro on the time-dependent increase in thrombin activityand platelet function have been used tocharacterize the kinetics of the clotting process in nonanticoagulated blood. The test procedures described involve great effort and expense and therefore are not suitable for routine tests in pharmacology and clinical pharmacology. The present contribution describes the determination of clotting times in ATP secretion in the Chrono-Log Whole Blood Aggregometer.Blood was taken from healthy donors who had not used any drug in the two weeks before the trial. 0.5 ml blood wereimmediately transfered into siliconizedglass cuvettes containing 0.4 ml salineand 0.1 ml luciferin-luciferase cocktail prewarmed to 37°C. Impedance and luminescence were recorded continuously. Clotting at the electrodes is indicated by an immediate steep rise in both impedance and luminescence. Clotting time is defined as the time from diluting the blood in the cuvettes until the point at which marked elevation of these variables begins.In the blood of twelve subjects the mean clotting time was 3.8 min and intersubject variation (SD) was 0.45 min. Drastic interindividual differences in response to collagen and ADP in citratedwhole blood were observed in the study group.In vitro addition of 20 μl Fibraccel(Behringwerke AG, Marburg, FRG),a platelet factor 3 containing plateletextract decreased clotting time by 35 %(n=10). In the presence of 0.2 U heparin a slow and lona-lasting increase in impedance was seen. 1 g oral AspirinR didnot influence clotting time measured ex vivo.The results indicate that whole blood aggregometry is a simple, fast, and precise method of determining blood clotting and the effects of drugs in a medium reflecting almost physiological conditions.
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Mackie, I. J., D. Bihari, and S. J. Machin. "INCREASED PLATELET AGGREGABILITY IN NATIVE WHOLE BLOOD IN THE ADULT RESPIRATORY DISTRESS SYNDROME (ARDS)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643477.
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The measurement of aggregation in whole blood allows the study of platelets in their natural milieu, but may still have anticoagulant induced artifacts; citrate decreases extracellular (Ca++) and heparin activates platelets. A technique for measuring aggregation in unanticoagulated (native) whole blood (NWB) was developed; blood is diluted in prewarmed saline with and without platelet agonists and aggregation is monitored by electrical impedance. Spontaneous and collagen induced aggregation were measured and the effect of prostacyclin analogue ZK 36,374 studied. The time until response (lag), aggregation rate, and clotting time were measured. Normal blood gave a cv of <7% for the NWB parameters; collagen gave a shorter lag and higher rate than in citrated whole blood (CWB). The lag and rate were inhibited in a dose dependent manner by ZK 36,374. 6 patients were studied on admission with ARDS and followed for several days. All had increased aggregation to collagen, which was more pronounced in NWB than CWB. A shortened lag was seen in some patients, but none showed spontaneous aggregation. ARDS patients showed no inhibition to ZK 36,374, and the heightened aggregation was not influenced by 2mM ASA, or normal plasma, while 2.5mM EDTA abolished all responses. Serum thromboxane B2 was normal, and increased flux through the cyclo-oxygenase pathway therefore unlikely. A parallel study has shown very low levels of antithrombin III (ATIII) in these patients, which may mean an increased thrombin generation rate with more thrombin available for platelet activation. This partly explains the difference in degree of hyperaggregability seen with NWB and CWB. During recovery from ARDS, collagen aggregation and the response to ZK 36,374 normalises at the same time as AT-III increases.
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Borowska, A., D. Lauri, A. Maggi, E. Dejana, G. de Gaetano, and J. Pangrazzi. "IMPAIREMENT OF PRIMARY HAEMOSTASIS BY LMW-HEPARINS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643172.
Full textAbstract:
Low molecular weight (LMW) heparlns have been developed with the aim of reducing anticoagulant activity thereby minimizing the bleeding complications of conventional heparin. Unexpectedly, bleeding events were reported during treatment with some LMW-heparins, in clinical and experimental studies. We studied the effect of four different LMW-heparlns on primary haemostasis In male rats (CD COBS, Charles River) after l.v. administration of 0.75 mg/kg b.w. of the drugs. LMW heparin A was devoid of any activity on an experimental model of “template” bleeding time in rats (110.6±5.9 sec versus 108.7±4.1 control values) whereas LMW-heparins B, C and D prolonged the bleeding time to a different extent (228.7±19.9, 161.5±6.4 and 161.7±8.6 respectively). Pretreatment of animals with aspirin (100 mg/kg b.w. per o.s). resulted In a significant potentiation of the “template” bleeding time. In vitro platelet aggregation Induced by collagen (20 μg/ml) or by collagen in combination with ADP (5-10 μM) was strongly inhibited by LMW-heparln B, while LMW-heparln A showed no effect. LMW-heparins C and D exerted an Intermediate level of Inhibition of platelet aggregation. The same pattern of aggregating response was found when LMW-heparins A and B were given i.v. to rats (0.75 mg/kg b.w.) and platelet aggregation was studied “ex vivo” 15 min after drug administration.These data may help explain the impairment of primary haemostasis associated with some LMW-heparin preparations.
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Boda, Z., G. Pfliegler, I. Tornai, M. Udvardy, J. Hársfalvi, and K. Rak. "LONG-TERM COUMAROL PLUS SMALL DOSE ASA THERAPY IN PATIENTS WITH PROSTHETIC HEART VALVE. SOME QUESTIONS OF LABORATORY CONTROL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643268.
Full textAbstract:
Thromboembolism in patients with prosthetic heart valves remains a major time-related problem (Sullivan 1971, Dale 1976, Chesebro 1983). Patients receiving anticoagulant plus antiplatelet agent have the lowest incidence of thromboembolism but the risk of bleeding is not negligible. The laboratory control of combined therapy is unsolved.This study considers the thromboembolic prophylaxis of 38 patients with prosthetic heart valve. Cou-marol treatment was combined with ASA (1 000 mg/week, 36 months follow up).Prothrombin ratio was used in control of the oral anticoagulant therapy. Malondialdehyde production was measured parallel with the so-called malondialdehyde-ratio (MDA-ratio = malondialdehyde level of patient/ control plasma). MDA-ratio, platelet aggregation, thromboxane and prostacycline metabolites were studied 48 hours after 500 mg ASA intake. The average of MDA-ratio was 0.42 ± 0.23 (from 137 measurements). The therapeutic range of MDA-ratio is 0.7 - 0.2. Value below 0.2 means overdosed, over 0.7 means an ineffective ASA therapy. Normal first and second phase platelet aggregation was observed in 23 % of cases when MDA-ratio was below 0.5. Only in 4 % of patients with MDA-ratio over 0.7 was found an abnormal platelet aggregation. The mean prothrombin ratio was 1.59 ± 0.22.No gastrointestinal bleeding or thromboembolism was observed during the 36 months follow up. Contrary to the literary data (Chesebro 1983) coumarol plus small dose ASA did not result excessive bleeding and can be suggested for patients with prosthetic heart valve. Examination of both the prothrombin and the malondialdehyde ratio with study of platelet aggregation is recommended as laboratory control.
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Sheriff, Jawaad, Michalis Xenos, João S. Soares, Jolyon Jesty, and Danny Bluestein. "Evaluation of Platelet Activation Models With Dynamic Shear Stress In Vitro Experiments." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80134.
Full textAbstract:
Blood recirculating devices, which include ventricular assist devices and prosthetic heart valves, are necessary for some patients suffering from end-stage heart failure and valvular diseases. However, disturbed flow patterns in these devices cause shear-induced platelet activation and aggregation. Thromboembolic complications resulting from this platelet behavior necessitates lifelong anticoagulant therapy for patients implanted with such devices. In addition, blood recirculating device manufacturers mostly test and optimize their products for hemolysis, which occurs at shear stresses ten-fold higher than required for platelet activation. The relative paucity of optimization for flow-induced thrombogenicity is further exacerbated by the fact that there are few predictive shear-induced platelet activation models.
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McKernan, A., J. M. Thomson, and L. Poller. "A PROSPECTIVE RANDOMISED CONTROLLED STUDY OF MINI-DOSE WARFARIN PROPHYLAXIS OF DEEP VEIN THROMBOSIS IN MAJOR SURGERY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643879.
Full textAbstract:
A prospective randomised study has been undertaken to assess the clinical effectiveness of oral anticoagulation using minidose warfarin (1 mg daily for 2-4 weeks before major gynaecological surgery) compared with conventional oral anticoagulant prophylaxis and an untreated randomised control group. The conventional oral anticoagulant prophylaxis was based on a therapeutic range of 1.5 - 2.0 INR at the time of operation and 2.0 - 3.0 INR post-operatively. Overall the mini-dose warfarin group showed no pre-operative prolongation of the prothrombin time with the Manchester Reagent although a minority of patients showed a 1-2 second prolongation of the prothrombin time before operation. Post operatively the mini-dose warfarin group showed an exaggerated prolongation of the prothrombin time which normally occurs after operation and was observed in the untreated controls. Factor VII assays paralleled these findings. Minidose warfarin, while not prolonging the prothrombin time before operation, resulted in delayed platelet aggregation with the Chandler's tube technique in almost all patients.The incidence of deep vein thrombosis has been reduced in both mini-dose and conventional dose oral anticoagulant series compared with the untreated- group. It appears that the minimal changes in the prothrombin time, factor VII and platelet aggregation tests, observed in the mini-dose warfarin group, may offer sufficient protection against post-operative thrombosis in a moderate risk group undergoing abdominal or pelvic surgery.