Relevant bibliographies by topics / Aspirin and platelet

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Aspirin and platelet'

Author: Grafiati
Published: 3 June 2025
Last updated: 31 July 2025

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Journal articles on the topic "Aspirin and platelet"

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Zhao, Lili, Weilin Zhang, Mengxing Chen, et al. "Aspirin Induces Platelet Apoptosis." Blood 120, no. 21 (2012): 5144. http://dx.doi.org/10.1182/blood.v120.21.5144.5144.

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Abstract Abstract 5144 Aspirin is widely used in the treatment of a number of clinical conditions, such as fever, pain, strokes, and heart attacks. Although aspirin is being thought of a relatively “safety” medicine, it also has some side effects, particularly the risk of bleeding which may be severe and lead to death. The mechanisms, however, are not totally understood. The effectiveness of aspirin has been attributed to its ability to inhibit prostaglandin production by inhibiting the cyclooxygenase (COX) enzyme. Interestingly, it has been reported recently that aspirin induces apoptosis in
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Alemanno, Laura, Isabella Massimi, Vanessa Klaus, et al. "Impact of Multidrug Resistance Protein-4 Inhibitors on Modulating Platelet Function and High on-Aspirin Treatment Platelet Reactivity." Thrombosis and Haemostasis 118, no. 03 (2018): 490–501. http://dx.doi.org/10.1055/s-0038-1629920.

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AbstractPlatelet multidrug resistance protein 4 (MRP4) plays a modulating role on platelet activation. Platelet function and thrombus formation are impaired in MRP4 knockout mice models, and, among aspirin-treated patients, high on-aspirin residual platelet reactivity (HARPR) positively correlates with MRP4 levels. To better understand the effects of MRP4 on platelet function, the aim of this investigation was to assess the impact of cilostazol-induced inhibition of MRP4-mediated transport and assess aspirin-induced antiplatelet effects and rates of HARPR in human subjects.Cilostazol-dependent
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Schwartz, Kenneth A., Dianne Schwartz, Ved Gossain, Anjana Myneni, Peggy Nelson, and Anthony Defranco. "Diabetic Platelets Are Not Resistant to Aspirin Inhibition." Blood 116, no. 21 (2010): 3324. http://dx.doi.org/10.1182/blood.v116.21.3324.3324.

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Abstract Abstract 3324 A daily aspirin in patients with myocardial infarctions (MI) effectively reduces the risk of occlusive vascular disease by 25%. This protective effect is reduced or absent in diabetics possibly because aspirin induced inhibition of platelet function is diminished. We tested the hypothesis that the amount of aspirin induced inhibition of platelets in diabetics is decreased. Methods: Each subject was evaluated at 2 time points: off-aspirin and 2-hours after observed ingestion of a 325mg aspirin tablet. Platelets were stimulated in a light aggregometer with platelet prostag
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Williams, P. Claire, Marcus J. Coffey, Barbara Coles, et al. "In vivo aspirin supplementation inhibits nitric oxide consumption by human platelets." Blood 106, no. 8 (2005): 2737–43. http://dx.doi.org/10.1182/blood-2005-02-0664.

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AbstractAntiplatelet therapies improve endothelial function in atherosclerosis, suggesting that platelets regulate vascular nitric oxide (NO) bioactivity in vivo. Herein, washed platelets consumed NO on activation in an aspirin-sensitive manner, and aspirin enhanced platelet NO responses in vitro. To examine whether in vivo aspirin can inhibit platelet NO consumption, a double-blind placebo-controlled study was conducted. After a 2-week nonsteroidal anti-inflammatory drug (NSAID)–free period, healthy men were randomly assigned and administered aspirin (75 mg/d orally) or identical placebo for
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Schwartz, Kenneth A., Dianne E. Schwartz, Kimberly Barber, Mathew Reeves, and Anthony C. DeFranco. "Minimal Frequency of Aspirin Resistance after Observed Aspirin Ingestion." Blood 106, no. 11 (2005): 551. http://dx.doi.org/10.1182/blood.v106.11.551.551.

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Abstract Poor compliance is an important cause of aspirin resistance. Our goal was to investigate amount of aspirin induced inhibition of platelets independent of compliance. We investigated the net amount of aspirin induced inhibition of platelets by comparing Platelet Prostaglandin Agonist (PPA) stimulated platelet aggregations before, off aspirin, with the platelet inhibition that occurred 2 hours after observed aspirin ingestion. 217 post-myocardial infarction patients who had taken aspirin for at least 30 days were evaluated at two time points. The first time point was 7 days after they h
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Tailor, Anitaben, Katherine C. Wood, John L. Wallace, Robert D. Specian, and D. Neil Granger. "Roles of platelet and endothelial cell COX-1 in hypercholesterolemia-induced microvascular dysfunction." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 6 (2007): H3636—H3642. http://dx.doi.org/10.1152/ajpheart.01105.2006.

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Aspirin is a common preventative therapy in patients at risk for cardiovascular diseases, yet little is known about how aspirin protects the vasculature in hypercholesterolemia. The present study determines whether aspirin, nitric oxide-releasing aspirin (NCX-4016), a selective cyclooxygenase (COX)-1 inhibitor (SC560), or genetic deficiency of COX-1 prevents the inflammatory and prothrombogenic phenotype assumed by hypercholesterolemic (HC) venules. Aspirin or NCX-4016 (60 mg/kg) was administered orally for the last week of a 2-wk HC diet. COX-1-deficient (COX-1−/−) and wild-type (WT) mice wer
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Gentry, P. A., R. R. M. Tremblay, and M. L. Ross. "Failure of aspirin to impair bovine platelet function." American Journal of Veterinary Research 50, no. 6 (1989): 919–22. https://doi.org/10.2460/ajvr.1989.50.06.919.

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SUMMARY The effect of aspirin on bovine platelet function and thromboxane A2 (txa2) production in stimulated platelets was evaluated. A single dose of aspirin (100 mg/kg of body weight) was administered orally to Holstein cows, and blood samples were obtained before and at regular intervals for 7 days after treatment. The production of txa2 was assessed by measuring the stable metabolite thromboxane B2, using a specific radioimmunoassay. Within 4 hours of aspirin administration, the production of txa2 was significantly (P < 0.05) decreased, irrespective of whether collagen, adenosine diphos
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Chronos, Nicolas A. F., Darren J. Wilson, Sarah L. Janes, Ronald A. Hutton, Nigel P. Buller та Alison H. Goodall. "Aspirin Does Not Affect the Flow Cytometric Detection of Fibrinogen Binding to, or Release of α-Granules or Lysosomes from, Human Platelets". Clinical Science 87, № 5 (1994): 575–80. http://dx.doi.org/10.1042/cs0870575.

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1. Aspirin inhibits the conversion of arachidonic acid to thromboxane A2 which reinforces the effects of weak agonists such as ADP in platelets. 2. In this study the effect of aspirin (300 mg/day) on platelet agonist response was measured by whole blood flow cytometry of unfixed blood samples from normal subjects (n = 10), an assay that investigates aggregation-independent changes in the platelet. 3. Fibrinogen binding to unstimulated platelets or to platelets stimulated with ADP or thrombin was unaffected by aspirin. 4. Under the conditions of this assay, platelets undergo a partial degranula
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Gordy, Dominique, Richard Francis, and Elizabeth Stone. "Using an agonist panel and aggregation to assess antiplatelet therapy in mice." American Journal of Clinical Pathology 160, Supplement_1 (2023): S142. http://dx.doi.org/10.1093/ajcp/aqad150.306.

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Abstract Platelets play a crucial role in hemostasis. For cardiovascular and stroke prophylaxis, patients are commonly placed on either single or dual antiplatelet drugs, such as aspirin and/or clopidogrel. Here we outline a mouse model examining antiplatelet therapy and the resulting changes in platelet activation and aggregation. Using commercially available transgenic mice with platelets expressing green fluorescent protein (GFP) or red fluorescent protein (RFP), endogenous platelets were inhibited with a single, dual, or control antiplatelet treatment. We used 100µg aspirin/g mouse or 50µg
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Schaefer, Jordan, John Davis, and Kenneth A. Schwartz. "Pharmacodynamics of Platelet Inhibition with Aspirin: Feasibility for Detection of Suboptimal Platelet Inhibition." Blood 120, no. 21 (2012): 4361. http://dx.doi.org/10.1182/blood.v120.21.4361.4361.

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Abstract Abstract 4361 Introduction: Patients with diabetes mellitus and or metabolic syndrome may or may not be maximally protected from future vascular events with aspirin. To be maximally protected at least 90% of platelets should be inhibited by aspirin (aspirinated). Since platelet acetylation by aspirin is limited to the first 30 minutes after ingestion, in conditions associated with increased platelet production the percentage of aspirinated platelets could be diluted to less than 90% with the usual daily dosing. We studied the pharmacodynamics of aspirin inhibition of platelets to eval
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Dissertations / Theses on the topic "Aspirin and platelet"

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Li, Melissa. "Microfluidic system for thrombosis under multiple shear rates and platelet therapies." Diss., Georgia Institute of Technology, 2013. http://hdl.handle.net/1853/52154.

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Thrombosis is the pathological formation of platelet aggregates that cause stroke and heart attack\textemdash the leading causes of death in developed nations. Determining effective dosages for platelet therapies (e.g. aspirin, Integrilin, and Plavix) to prevent thrombosis is a persistent medical challenge (studies estimate up to 45% of patients exhibit insufficient responses to these drugs) and recent studies have implicated pathological flow conditions of high shear rates and stenosis morphology as primary factors. However, there are currently no diagnostic instruments able to recapitulate
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Navaratnam, K. "Platelet function and response to low-dose aspirin in pregnancy." Thesis, University of Liverpool, 2017. http://livrepository.liverpool.ac.uk/3009774/.

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Pre-eclampsia is a serious multisystem disorder unique to pregnant women and associated with significant maternal and perinatal morbidity and mortality worldwide. Despite the investment of decades of basic science and clinical research, the pathophysiology of pre-eclampsia has been incompletely illustrated. In low doses, the cyclooxygenase inhibitor and antiplatelet, aspirin, can redress the thromboxane/prostacyclin imbalance observed in pregnancies affected by pre-eclampsia. Low-dose aspirin is currently recommended for high risk pregnancies in many countries, despite affording only modest ov
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Cheng, Xi. "Prevalence, profile, predictors, and natural history of aspirin resistance measured by the ultegra rapid platelet function assay-asa in patients with coronary artery disease." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B33708708.

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Zhao, Lian. "Effects of antiplatelet agents on platelet and leucocyte function : from laboratory research to clinical practice." Thesis, University of Nottingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289062.

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Desborough, Michael J. R. "Desmopressin for treatment of thrombocytopenia or platelet dysfunction." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:4de19720-328a-4d01-9153-02dec6202aff.

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The objective of the work presented in this thesis was to explore the role of potential alternatives to platelet transfusions and specifically to investigate whether desmopressin could be used for treatment of thrombocytopenia or platelet dysfunction. Patients with thrombocytopenia or platelet dysfunction are often treated with platelet transfusions to treat or prevent bleeding. However the evidence for the efficacy of platelet transfusion is limited and there is some evidence of harm. I have focused on thrombocytopenic patients with haematological malignancies or critically ill patients, who
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Cheng, Xi, and 程曦. "Prevalence, profile, predictors, and natural history of aspirin resistance measured by the ultegra rapid platelet function assay-asain patients with coronary artery disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B33708708.

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Cassar, Kevin. "Management of secondary risk factors and the effects of combination aspirin clopidogrel on platelet function in claudicants." Thesis, University of Aberdeen, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288256.

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This research study consisted of three parts.  In the first part two surveys were conducted, one among General Practitioners (GPs) in Grampian Area of Scotland and the second among Consultant Vascular Surgeons throughout the United Kingdom and Ireland, which aimed to explore the attitudes towards management of secondary risk factors in patients with intermittent claudication.  Postal questionnaires were used to determine how GPs and Consultant vascular surgeons screened for and controlled the major risk factors - cigarette smoking, hypertension, diabetes and hyperlipidaemia, whether and what a
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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 (
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Turner, Lisa A. "Profiling Precursor Lipids for Specialized Pro-Resolution Molecules in Platelet-Rich Plasma Following Fish Oil and Aspirin Intake." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4763.

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Background: Unfavorable outcomes following periodontal surgeries can be attributed to impaired resolution mechanisms likely due to decreased levels of specialized pro-resolution molecules (SPM). The current study investigates if SPM substrate pools in platelet-rich plasma preparations (PRP) can be increased by essential fatty acid (EFA) and / or aspirin supplementation. Methods: Nineteen healthy volunteers were randomly assigned to take i) aspirin; ii) EFA; iii) aspirin and EFA. Four hours after intake, the lipid precursor pools in PRP were quantified using combined Liquid Chromatography tande
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McCormack, Danielle M. "Profiling Precursor Lipids for Specialized Pro-Resolution Molecules in Platelet-Rich Fibrin Following Fish Oil and Aspirin Intake." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4761.

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Background: Current research has demonstrated that aspirin and fish oil (EFA) increase plasma levels of specialized pro-resolution molecules (SPMs). This study investigates their effects on SPM precursor pools in platelet rich fibrin (PRF). Methods: Twenty healthy volunteers were randomly assigned to take aspirin; EFA or aspirin and EFA. Four hours later, SPM precursor levels were quantified using combined Liquid Chromatography tandem mass spectrometry. The differences between the groups: Aspirin (yes or no), EFA (yes or no), were analyzed by ANCOVA, testing for group differences after covaryi
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Books on the topic "Aspirin and platelet"

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Single Versus Dual Anti-Platelet Drug Therapy in the Management of Coronary Artery Disease, Adding Aspirin to Clopidogrel Versus Clopidogrel Alone. Independently Published, 2020.

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Wijdicks, Eelco F. M., and Sarah L. Clark. Antiplatelet Agents. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190684747.003.0009.

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Antiplatelet agents are commonly used in vascular medicine and cardiology, but also in the pharmacologic management of patients with ischemic stroke. Aspirin alone remains the mainstay of therapy for secondary stroke prevention. Several landmark studies for the optimal duration and dose of antiplatelet therapy in stroke prevention are discussed. Dual antiplatelet therapy is needed after carotid artery stenting. Situations where antiplatelet agents also come into play are endovascular procedures associated with procedure-related thrombi. Antiplatelet agents have different mechanisms of action,
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Platelets and Aspirin-Induced Asthma. Elsevier, 2014. http://dx.doi.org/10.1016/c2013-0-13454-x.

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Evsyukova, Helen. Platelets and Aspirin-Induced Asthma: Pathogenesis and Melatonin. Elsevier Science & Technology Books, 2013.

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Evsyukova, Helen. Platelets and Aspirin-Induced Asthma: Pathogenesis and Melatonin. Elsevier Science & Technology Books, 2013.

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Balik, Martin. Perioperative cardiac care of the high-risk non-cardiac patient. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0076.

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Non-cardiac surgery conveys a cardiac risk related to the status of the patient’s cardiovascular system. Cardiac-related risk of surgery can be assessed by integrating the risk and urgency of the procedure with cardiovascular risk factors, which include age, ischaemic heart disease, heart failure, stroke, diabetes mellitus, chronic obstructive pulmonary disease, and renal dysfunction. An individual assessment can include simple multivariate scoring systems, developed with the aim of evaluating cardiac risk prior to non-cardiac surgery. Patient assessment can be extended for indicated additiona
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Balik, Martin. Perioperative cardiac care of the high-risk non-cardiac patient. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0076_update_001.

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Non-cardiac surgery conveys a cardiac risk related to the status of the patient’s cardiovascular system. Cardiac-related risk of surgery can be assessed by integrating the risk and urgency of the procedure with cardiovascular risk factors, which include age, ischaemic heart disease, heart failure, stroke, diabetes mellitus, chronic obstructive pulmonary disease, and renal dysfunction. An individual assessment can include simple multivariate scoring systems, developed with the aim of evaluating cardiac risk prior to non-cardiac surgery. Patient assessment can be extended for indicated additiona
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Balik, Martin. Perioperative cardiac care of the high-risk non-cardiac patient. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0076_update_002.

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Non-cardiac surgery conveys a cardiac risk related to the status of the patient’s cardiovascular system. Cardiac-related risk of surgery can be assessed by integrating the risk and urgency of the procedure with cardiovascular risk factors, which include age, ischaemic heart disease, heart failure, stroke, diabetes mellitus, chronic obstructive pulmonary disease, and renal dysfunction. An individual assessment can include simple multivariate scoring systems, developed with the aim of evaluating cardiac risk prior to non-cardiac surgery. Patient assessment can be extended for indicated additiona
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Book chapters on the topic "Aspirin and platelet"

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Joseph, Michel, A. Capron, A. Tsicopoulos, J. C. Ameisen, J. B. Martinot, and A. B. Tonnel. "Platelet Activation by IgE and Aspirin." In PAF, Platelets, and Asthma. Birkhäuser Basel, 1987. http://dx.doi.org/10.1007/978-3-0348-7451-9_15.

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Calverley, David C., and Gerald J. Roth. "Aspirin, Prostaglandins and Platelet Function: Pharmacology and Thrombosis Prevention." In Handbook of Platelet Physiology and Pharmacology. Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5049-5_22.

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Patrono, Carlo. "Aspirin." In Platelets in Thrombotic and Non-Thrombotic Disorders. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47462-5_83.

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Ryan, J. R., F. G. McMahon, R. Vargas, et al. "Differential influences of salsalate, aspirin and naproxen on plasma renin activity and platelet thromboxane (TxB)2 synthesis." In Side-Effects of Anti-Inflammatory Drugs. Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-010-9775-8_48.

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Szczeklik, A. "Eicosanoids and Aspirin-Sensitive Asthma." In PAF, Platelets, and Asthma. Birkhäuser Basel, 1987. http://dx.doi.org/10.1007/978-3-0348-7451-9_17.

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von Pape, K. W., M. Dzijan-Horn, J. Bohner, M. Spannagl, H. Weisser, and A. Calatzis. "Control of Aspirin Effect in Chronic Cardiovascular Patients Using two Whole Blood Platelet Function Assays: PFA-100 and Multiple Electrode Aggregometry." In 36th Hemophilia Symposium Hamburg 2005. Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-36715-4_49.

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Nizankowska, Ewa, A. Q. Sheridan, M. H. Maile, C. J. Cross, G. Czerniawska-Mysik, and A. Szcezklik. "Pharmacological Attempts to Modulate Leukotriene Synthesis in Aspirin-Induced Asthma." In PAF, Platelets, and Asthma. Birkhäuser Basel, 1987. http://dx.doi.org/10.1007/978-3-0348-7451-9_18.

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de Gaetano, Giovanni, and Chiara Cerletti. "Blood Platelets, Aspirin and Prevention of Vascular Disease." In Prostanoids and Drugs. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-7938-6_9.

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Sörgel, F., H. Hopf, E. Lang, and M. Geldmacher von Mallinckrodt. "The response of human platelets to aspirin in vitro." In Side-Effects of Anti-Inflammatory Drugs. Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-010-9775-8_47.

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Becker, Richard C., and Frederick A. Spencer. "Aspirin." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0012.

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Aspirin, considered the prototypic platelet antagonist, has been available for over a century and currently represents a mainstay both in the prevention and treatment of vascular events that include stroke, myocardial infarction, peripheral vascular occlusion, and sudden death. Aspirin irreversibly acetylates cyclooxygenase (COX), impairing prostaglandin metabolism and thromboxane A2 (TXA2) synthesis. As a result, platelet aggregation in response to collagen, adenosine diphosphate (ADP), and thrombin (in low concentrations) is attenuated (Roth and Majerus, 1975). Because aspirin more selective
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Conference papers on the topic "Aspirin and platelet"

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Cordova, C., F. Violi, D. Praticò, A. Ghiselli, C. Alessandri, and F. Balsano. "CYCLOOXYGENASE INDIPENDENT PLATELET AGGREGATION:RELATION WITH ASPI RIN CONCENTRATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644828.

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Low doses of aspirin (20 mg/day) were previously reported to be uneffective in preventing platelet aggregation (PA) induced by pairs of aggregating agents such as PAF and adrenalin.This was in part attributed to the inability of such treatment to inhibit lipo oxygenase-dependent PA.The latter can be observed in vitro in"aspl rinated"platelets stimulated with high quantities of aggregating -agents.The aim of this study was to evaluate if the lipooxygenase-dependent PA was influenced by aspirin in a dose-dependent fashion. PA was studied in platelet rich plasma (PRP)(Born's method) by using thre
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Woods, A. I., and Ji A. Lazzari. "ASPIRIN EFFECT ON PLATELET ANTIPLASMINS PRELEASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643497.

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It was shown platelet antiplasmin activity which is released by col 1anen(Col)and thrombin, probably associated with a-oran u 1 es . Lys i s area produced by eunl obul i ns (eun) of PPP and PRP whether or not previously treated with ADP(5uM), Col(20ug/ml) and aspirin(ASA)(00up/nl)in plas-mi nooen- f ree-f i bri n plates were s tudi ed. Res u 1 ts (mm2 ) were:eunPPP:151.3±39.8;+ADP:155.7±47;+Co1: 155.5±150.8; + ASA: 160±142. -EugPRP: 142*42;+ADP: 145*72;+Col : 136*43 ; -⋋ASA: 138+47.-EugPRP produced slightly lower lysis area than euaPPP(p:ns).ADP , Co 1 and ASA neither modify the lysis area of
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Lloyd, J. V., S. E. Rodgers, D. M. Siebert, F. Bochner, G. H. McIntosh, and M. James. "PRESYSTEMIC DEACETYLATION OF LOW DOSES OF ENTERIC COATED ASPIRIN IN A PIG MODEL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643856.

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The antithrombotic effect of aspirin might be enhanced if platelet cyclooxygenase could be inhibited in the portal ciculation while sparing cyclooxygenase in the systemic vascular endothelium. This might be achieved by modifying the dose and formulation to maximise presystemic aspirin clearance by the liver. To test this hypothesis low dose enteric coated aspirin (Astrix, 50mg single dose, lOOmg single dose and lOOmg daily for 1 week) was orally administered to pigs with permanent indwelling arterial and portal vein catheters. Plasma aspirin concentrations were measured by high performance liq
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Santos, M. T., J. Aznar, J. Valles, and J. L. Perez-Reguejo. "ASPIRIN MODIFIES RED BLOOD CELL BEHAVIOUR (RBC) IN THE PLATELET-RBC INTERACTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644821.

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RBC stimulate the initial stages of platelet activation by collagen as evaluated by the BASIC wave (Perez-Requejo et al. Thromb Haemostas 54:799 1985). In order to get some insight into the mechanisms of platelet-RBC interactions, a BASIC wave was induced by lug/ml of collagen after mixing "in vitro" platelets and RBC obtained both before and two hours after a single dose of 500 mg of ASA from normal subjects. The TXB2 formed was also evaluated. The results show (Table) that non aspirinized RBC (non-ASA-RBC) increase the BASIC wave intensity of aspirinized platelets (ASA-PRP) by a cyclooxygena
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Mazurov, A. V., V. E. Si-nitsin, and V. S. Repin. "HEPARIN POTENTIATES PLATELET ADHESION AND AGGREGATION ON COLLAGEN SUBSTRATES. ABSENCE OF INHIBITION BY ASPIRIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644183.

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We studied the effects of two commercial heparin (H) preparations, from bovine lungs (HL) and pig intestine (HI), on the interaction of human plateletswith collagen substrates, and tested a possibility of modulating these effects by aspirin. PRP was incubated in the presence or absence of H with human collagens type IV and III (CIV and Cl I I) adsorbed ona plastic surface. Platelet adhesion and spreading on CIV and aggregation on Cl I I was quantitated by scanning electron microscopy. HL and HI were added to platelets in the concentrations approximating to those achieved in vivo at heparin the
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Matsuo, T., T. Yamada, and K. Nakao. "EFFECT OF A SYNTHETIC ANTICOAGULANT (MD 805) ON PLATELETS IN HUMAN VOLUNTEERS AND HEMODIALYSIS PATIENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643457.

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Twelve normal subjects were injected with 5000 U of commercial mucous heparin with or without preloading of 1.0 g aspirin, and 0.2 mg/kg MD 805, an arginine derivative, which is a new synthetic compound with an extremely strong affinity for thrombin, at an interval of 4 weeks after each injection. Heparin injection with or without aspirin significantly increased platelet factor 4 release. In contrast, the preloading of aspirin significantly inhibited the decrease of platelet count and the elevation of /8 thromboglobulin induced by heparin. However, MD 805 had no effect on platelet release prot
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Gladwin, A. M., and J. Martin. "ARACHIDONIC ACID (AA) INDUCED AGGREGATION OF RAT PRO- MEGAKARYOBLASTS (RPM)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643542.

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Platelet aggregation can be induced in vitro by a variety of platelet agonists acting upon membrane receptors. Since platelets have only a limited ability to synthesise proteins, these receptors must be present in megakaryocytes. This was investigated using an eternal line line of RPMs. Cells were suspended in rat platelet free plasma (PFP) at a concentration of 105 cells ml-1 . 200μl aliquots of this were placed in a light aggregometer. For this suspension, and for an aliquot of PFP, light transmission was adjusted to zero and 100% respectively. Addition of ADP (plasma concentrations 1-100μM)
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patrono, C. A. "CLINICAL TRIALS OF ANTITHROMBOTIC AGENTS IN UNSTABLE ANGINA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643713.

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A Veterans Administration (VA) Cooperative Study (NEJM 309:396,1983) has demonstrated that a single daily administration of aspirin 324 mg in buffered solution, started within 51 hours of admission to the hospital, significantly reduced the 12-week incidence of acute myocardial infarction (MI) or death by 51% in men with unstable angina. These results have been substantially confirmed by a Canadian Multicenter Trial (NEJM 313:1369,1985) in patients of both sexes treated with aspirin 325 mg qid. The rate of death or acute MI wasfound to be 51% lower in the group treated with aspirin,after a mea
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Backhouse, C. M., A. C. Meek, K. R. Poskitt, and C. N. McCollum. "PULMONARY MICROEMBOLISATION IN SURGICAL SHOCK: THE EFFECT OF CYCLO-OXYGENASE INHIBITION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643458.

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Thromboxane release from platelet microemboli during major arterial surgery may mediate depression of cardio-pulmonary function. The effect of cyclo-oxygenase inhibition by aspirin has been studied in a porcine model of aortic surgery.Following autologous platelet labelling with 111-lndium, 24 pigs (20-25kg) were randomised to low dose (LD) aspirin (0.5mg/kg), high dose (HD) aspirin (10mg/kg) or placebo.Arterial and Swann Ganz catheters were inserted prior to surgery consisting of midline laparotomy, small bowel extériorisation, 1.5 hours of aortic clamping and 1 hour shock before resuscitatio
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Cerletti, C., M. C. Gombino, S. Possaghe, F. Bucchi, Z. M. Chen, and G. de Gaetano. "EFFECTS OF ORAL ASPIRIN ON PLATELET AND VASCULAR CYCLOOXYGENASE ACTIVITY IN RATS WITH PORTACAVAL SHUNT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643417.

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Oral aspirin can be extensively hydrolysed to salicylate in stomach and liver before entering the systemic circulation. “Pre-systemic” acetylation of the platelets may thus occur during aspirin absorption. This may result in concomitant sparing of peripheral vascular cyclooxygenase mainly exposed to salicylate. We tested whether the “biochemical selectivity” of oral aspirin as an inhibitor of platelet vs. vascular cyclooxygenase would be reduced by elimination of the “first-pass” hepatic metabolism. A portacaval shunt was inserted in anaesthetized rats by connecting the portal vein to the infe
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