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Journal articles on the topic 'Aspirin and platelet'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

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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2

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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3

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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4

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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9

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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10

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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11

Massimi, Isabella, Lavinia Lotti, Flavia Temperilli, et al. "Enhanced platelet MRP4 expression and correlation with platelet function in patients under chronic aspirin treatment." Thrombosis and Haemostasis 116, no. 12 (2016): 1100–1110. http://dx.doi.org/10.1160/th16-04-0316.

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SummaryPlatelet multidrug resistance protein4 (MRP4)-overexpression has a role in reducing aspirin action. Aspirin in vivo treatment enhances platelet MRP4 expression and MRP4 mediated transport inhibition reduces platelet function and delays thrombus formation. The aim of our work was to verify whether MRP4 expression is enhanced in platelets obtained from patients under chronic aspirin treatment and whether it correlates with residual platelet reactivity. We evaluated changes on mRNA and protein-MRP4 expression and platelet aggregation in four populations: healthy volunteers (HV), aspirin-fr

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Dropinski, Jerzy, Bogdan Jakiela, Marek Sanak, et al. "The additive antiplatelet action of clopidogrel in patients with coronary artery disease treated with aspirin." Thrombosis and Haemostasis 98, no. 07 (2007): 201–9. http://dx.doi.org/10.1160/th06-12-0722.

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SummaryWe searched for additional anti-platelet effects of clopidogrel in coronary artery disease (CAD) patients treated with aspirin. Response to clopidogrel was also stratified according to aspirin resistance. Out of 76 screened aspirin-treated CAD male patients, five were aspirin-resistant based on arachidonic acid (AA) and ADP aggregometry.These five patients and 15 aspirin-sensitive patients entered the proper study. Platelet function was assessed at baseline and after one week of additional clopidogrel treatment using aggregometry, flow cytometry (ADP, TRAP-6) and platelet reactivity ind

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Chen, Hung Yi, and Pesus Chou. "Associations Between PFA-Measured Aspirin Resistance, Platelet Count, Renal Function, and Angiotensin Receptor Blockers." Clinical and Applied Thrombosis/Hemostasis 24, no. 9_suppl (2018): 63S—68S. http://dx.doi.org/10.1177/1076029618786588.

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Aspirin resistance is used to describe patients who are undergoing aspirin therapy but fail for the inhibition of thromboxane biosynthesis in platelets. Although the true mechanism is unclear, drug–drug interaction remains a possible factor. The study aimed to determine whether there was association between aspirin resistance and the concomitant cardiovascular medication. Using the Platelet Function Analyzer-100 system, aspirin resistance was evaluated in aspirin-treated patients from the outpatient department. The associations between aspirin resistance and their concomitant common cardiovasc

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Sils, D., S. E. Rodgers, J. V. Lloyd, K. M. Wilson, D. M. Siebert, and F. Bochner. "Inhibition of platelet aggregation and thromboxane production by low concentrations of aspirin in vitro." Clinical Science 74, no. 5 (1988): 491–97. http://dx.doi.org/10.1042/cs0740491.

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1. The aspirin concentrations previously reported to inhibit platelet aggregation in vitro (40–500 μmol/l) are much greater than those required in vivo in man (5 μmol/l). 2. Human platelet-rich plasma was incubated with buffer or various aspirin concentrations at 37°C for up to 4.5 h. Platelet aggregation and thromboxane generation were measured in response to collagen (0.4–6.3 μg/ml) and adenosine 5′-pyrophosphate (0.5–4 μmol/l). 3. The concentration of aspirin needed to inhibit platelet aggregation in response to a critical concentration of aggregating agent (lowest concentration to cause gr

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15

Polzin, Amin, Betül Knoop, Andreas Böhm, et al. "Aspirin Inhibits Platelet-Derived Sphingosine-1-Phosphate Induced Endothelial Cell Migration." Pharmacology 101, no. 1-2 (2017): 72–75. http://dx.doi.org/10.1159/000484208.

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Background: Aspirin plays a crucial role in the prevention of cardiovascular diseases. We previously described that aspirin has effects beyond inhibition of platelet aggregation, as it inhibited thrombin-mediated release of sphingosine-1-phosphate (S1P) from human platelets. S1P is a bioactive lipid with important functions on inflammation and apoptosis. In endothelial cells (EC), S1P is a key regulator of cell migration. In this study, we aimed to analyze the effects of aspirin on platelet-induced EC migration. Methods: Human umbilical EC migration was measured by Boyden chamber assay. EC mig

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Morotti, Alessandro, Cristina Barale, Michele Sornatale, et al. "Aberrant Platelet Aggregation as Initial Presentation of Essential Thrombocythemia: Failure of Entero-Coated Aspirin to Reduce Platelet Hyperactivation." International Journal of Molecular Sciences 25, no. 1 (2023): 176. http://dx.doi.org/10.3390/ijms25010176.

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Essential thrombocythemia (ET) is a myeloproliferative neoplasm variant characterized by excessive production of platelets. Since the most common cause of mortality and morbidity in ET patients is thrombosis, the excessive production of platelets may cause thrombotic events. However, little is known about the function of platelets in ET. We report a female patient who presented as asymptomatic, without a remarkable medical history, and ET was diagnosed after an incidental finding of moderate thrombocytosis. Notably, together with thrombocytosis, an abnormal platelet phenotype was found for the

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Berent and Sinzinger. "Aspirin - resistance? A few critical considerations on definition, terminology, diagnosis, clinical value, natural course of atherosclerotic disease, and therapeutic consequences." Vasa 40, no. 6 (2011): 429–38. http://dx.doi.org/10.1024/0301-1526/a000145.

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Based upon various platelet function tests and the fact that patients experience vascular events despite taking acetylsalicylic acid (ASA or aspirin), it has been suggested that patients may become resistant to the action of this pharmacological compound. However, the term aspirin resistance was created almost two decades ago but is still not defined. Platelet function tests are not standardized, providing conflicting information and cut-off values are arbitrarily set. Intertest comparison reveals low agreement. Even point of care tests have been introduced before appropriate validation. Inf

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Schwartz, Kenneth A., John Davis, and Jordan Schaefer. "A Light Aggregometry Based Method To Measure The Percentage Of An Individual’s Platelets That Are Inhibited By Aspirin." Blood 122, no. 21 (2013): 2390. http://dx.doi.org/10.1182/blood.v122.21.2390.2390.

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Abstract Background Ex-vivo analysis of platelet inhibition by aspirin (ASA) suggests that an optimal decrease in platelet function occurs when 90-95% of platelets are inhibited with ASA. In patients with known vascular disease a daily aspirin decreases the probability of a future vascular event by about 25%. However, platelets from patients with diabetes mellitus (DM) are highly reactive with an increased turnover rate, and prophylaxis with a daily aspirin is not nearly as effective. Because platelet response among individuals is highly variable, we developed a light aggregation based assay t

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Schwartz, Kenneth A., Dianne E. Schwartz, Anjana Myneni, Peggy Nelson, and Ved Gossain. "Inhibition of Platelet Function by Aspirin in Insulin Dependent Diabetics without Vascular Disease." Blood 114, no. 22 (2009): 4172. http://dx.doi.org/10.1182/blood.v114.22.4172.4172.

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Abstract Abstract 4172 Diseases like diabetes that are associated with increased platelet production are reported to have decrease aspirin (ASA) induced platelet inhibition. ASA inhibition of platelet function is mediated via acetylation of platelet cylooxygenase, which is completed approximately 30 minutes after ingestion. Thereafter production of new non-acetylated platelets increases the proportion of normal platelets gradually reversing ASA platelet inhibition. We tested the hypothesis that insulin dependent diabetics (type 1) without clinical evidence of occlusive vascular disease have le

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Johnson, Kelly E., Julia R. Ceglowski, Harvey G. Roweth, et al. "Aspirin inhibits platelets from reprogramming breast tumor cells and promoting metastasis." Blood Advances 3, no. 2 (2019): 198–211. http://dx.doi.org/10.1182/bloodadvances.2018026161.

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Abstract It is now recognized that compounds released from tumor cells can activate platelets, causing the release of platelet-derived factors into the tumor microenvironment. Several of these factors have been shown to directly promote neovascularization and metastasis, yet how the feedback between platelet releasate and the tumor cell affects metastatic phenotype remains largely unstudied. Here, we identify that breast tumor cells secrete high levels of interleukin 8 (IL-8, CXCL8) in response to platelet releasate, which promotes their invasive capacity. Furthermore, we found that platelets

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Xu, Xiaohong Ruby, George M. Yousef, and Heyu Ni. "Cancer and platelet crosstalk: opportunities and challenges for aspirin and other antiplatelet agents." Blood 131, no. 16 (2018): 1777–89. http://dx.doi.org/10.1182/blood-2017-05-743187.

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Abstract Platelets have long been recognized as key players in hemostasis and thrombosis; however, growing evidence suggests that they are also significantly involved in cancer, the second leading cause of mortality worldwide. Preclinical and clinical studies showed that tumorigenesis and metastasis can be promoted by platelets through a wide variety of crosstalk between platelets and cancer cells. For example, cancer changes platelet behavior by directly inducing tumor-platelet aggregates, triggering platelet granule and extracellular vesicle release, altering platelet phenotype and platelet

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Kaplan, Alexander, Svetlana Kaplan, Karen F. Marcoe, Lester R. Sauvage, and William P. Hammond. "Modified Technique for Measuring Platelet Aggregation." Clinical and Applied Thrombosis/Hemostasis 3, no. 3 (1997): 196–202. http://dx.doi.org/10.1177/107602969700300308.

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The turbidimetric method of Bom is the current approach for assessing the aggregation behavior of platelets. It has been of modest practical value, due to difficulty in standardizing laboratory techniques for plasma preparation and inadequate quantification of the aggregation process. We report a new technique of sedimented platelet rich plasma (SPRP) preparation that reduces the irregularities caused by factors associated with procuring and preparing blood samples and permits a more flexible protocol for laboratory practice. We quantified results with a platelet aggregation score, which is ca

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Mykhaloiko, O. "Changes in platelet counts in patients with acute ischemic stroke depending on sensitivity to acetylsalicylic acid therapy." Bukovinian Medical Herald 24, no. 4 (96) (2020): 65–74. http://dx.doi.org/10.24061/2413-0737.xxiv.4.96.2020.105.

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The study aims to investigate changes in the thrombocytogram in patients with early recovery from ischemic stroke depending on the sensitivity to acetylsalicylic acid therapy.Material and methods. A clinical and laboratory analysis of 80 patients with acute ischemic stroke (AII), who took acetylsalicylic acid (ASA) at a dose of 75-100 mg per night to prevent recurrent stroke. The control group consisted of 30 healthy individuals who did not take ASA. The functional activity of platelets was determined on a laser aggregometer Biola Aggregation Analyzer and on the results of a platelet cytogram

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Guthikonda, Sasidhar, Kirankumar Mangalpally, Rajnikant Patel, et al. "Increased platelet sensitivity among individuals with aspirin resistance – Platelet aggregation to submaximal concentration of arachidonic acid predicts response to antiplatelet therapy." Thrombosis and Haemostasis 100, no. 07 (2008): 83–89. http://dx.doi.org/10.1160/th07-10-0590.

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SummaryAspirin ‘resistance’ (AR) is a phenomenon of uncertain etiology describing decreased platelet inhibition by aspirin. We studied whether (i) platelets inAR demonstrate increased basal sensitivity to a lower degree of stimulation and (ii) platelet aggregation with submaximal stimulation could predict responses to aspirin. Serum thromboxane B2 (TxB2) levels and platelet aggregation with light transmission aggregometry (LTA ) were measured at baseline and 24 hours after 325 mg aspirin administration in 58 healthy subjects. AR was defined as the upper sixth of LTA (≥ 12%) to 1.5 mM AA. Basel

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Massimi, Isabella, Laura Alemanno, Maria Guarino, et al. "Aspirin-Dependent Effects on Purinergic P2Y1 Receptor Expression." Thrombosis and Haemostasis 119, no. 05 (2019): 726–34. http://dx.doi.org/10.1055/s-0039-1678707.

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AbstractChronic treatment with aspirin in healthy volunteers (HVs) is associated with recovery of adenosine diphosphate (ADP)-induced platelet activation. The purinergic P2Y1 receptor exerts its effects via a Gq-protein, which is the same biochemical pathway activated by thromboxane-A2 receptor. We hypothesized that recovery of ADP-induced platelet activation could be attributed to increased P2Y1 expression induced by chronic aspirin exposure. We performed a multi-phase investigation which embraced both in vitro and in vivo experiments conducted in (1) human megakaryoblastic DAMI cells, (2) hu

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Moscardó, Antonio, María Paz Fuset, Miguel Ruano, María Teresa Santos, and Juana Vallés. "Residual cyclooxygenase-1 activity and epinephrine reduce the antiplatelet effect of aspirin in patients with acute myocardial infarction." Thrombosis and Haemostasis 105, no. 04 (2011): 663–69. http://dx.doi.org/10.1160/th10-08-0550.

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SummaryAspirin treatment is essential in patients with acute myocardial infarction (AMI) to block platelet thromboxane (TXA)2 synthesis. Epinephrine is known to enhance platelet reactivity induced by other agonists and to be elevated in patients with AMI due to stress. Our objective was to study the influence of epinephrine on platelet TXA2 synthesis in patients treated with aspirin for AMI at early onset (within 48 hours) and the potential biochemical mechanisms involved in the functional response. Washed platelets from 45 patients with AMI and 10 aspirin-free controls were stimulated with ar

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Sabaliauskienė, Zita, Pranas Grybauskas, and Virginija Gaigalaitė. "The impact of acute cerebral blood flow disturbances on platelet aggregation." Medicina 44, no. 12 (2008): 922. http://dx.doi.org/10.3390/medicina44120115.

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Objective. To determine the changes in platelet function, manifesting as deviations of their aggregation intensity, in persons with acute ischemic stroke and transient ischemic attacks, to evaluate the effect of aspirin on platelet aggregation, dependent upon degree of cerebral blood flow disturbances and patient’s gender, and to compare these changes with those in healthy persons. Material and methods. We examined 50 patients aged 33 to 98 years (mean age, 63.7±2.1 years; 20 men and 30 women) with cerebral blood flow disturbances during acute period (18 with transient ischemic attacks and 32

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Hechtman, D. H., M. H. Kroll, M. A. Gimbrone, and A. I. Schafer. "Platelet interaction with vascular smooth muscle in synthesis of prostacyclin." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 5 (1991): H1544—H1551. http://dx.doi.org/10.1152/ajpheart.1991.260.5.h1544.

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Because vascular smooth muscle cells (SMC) can be exposed to platelets at sites of significant arterial injury, we studied whether cultured rat aorta SMC can utilize platelet-derived arachidonate and prostaglandin (PG) endoperoxides (PGG2/PGH2) in the synthesis of prostacyclin (PGI2). SMC converted exogenous PGH2 to PGI2, measured by radioimmunoassay (RIA) of 6-keto-PGF1 alpha, despite cyclooxygenase inhibition or PGH2-receptor blockade. SMC produced increasing amounts of PGI2 in the presence of an increasing number of platelets when the two cell types were coincubated with arachidonate. Furth

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Kuliczkowski, Wiktor, Marek Radomski, Mariusz Gąsior, et al. "MMP-2, MMP-9, and TIMP-4 and Response to Aspirin in Diabetic and Nondiabetic Patients with Stable Coronary Artery Disease: A Pilot Study." BioMed Research International 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/9352015.

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Background. High on-aspirin treatment platelets reactivity (HPR) is a significant problem in long-term secondary prevention of cardiovascular events. We hypothesize that imbalance between platelets MMPs/TIMPs results in cardiovascular disorders. We also explored whether chronically elevated blood glucose affects MMP-2/TIMP-4 release from platelets. Materials and Methods. Seventy patients with stable coronary artery disease, supplemented with aspirin, participated in this pilot study. The presence of HPR and/or diabetes mellitus was considered as the differentiating factor. Light aggregometry,

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Rinder, CS, LA Student, JL Bonan, HM Rinder, and BR Smith. "Aspirin does not inhibit adenosine diphosphate-induced platelet alpha- granule release." Blood 82, no. 2 (1993): 505–12. http://dx.doi.org/10.1182/blood.v82.2.505.505.

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Abstract The involvement of metabolites of arachidonic acid in platelet-dense granule secretion and secondary platelet-platelet interactions is well characterized. However, their role in heterotypic interactions dependent on alpha-granule secretion is less well understood. Using platelet-surface expression of P-selectin as a marker of alpha-granule secretion, we have shown that: (1) aspirin treatment of platelets at doses that block dense granule secretion does not inhibit alpha-granule secretion to adenosine diphosphate (ADP); (2) synergism between epinephrine and ADP in the induction of P-se

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Rinder, CS, LA Student, JL Bonan, HM Rinder, and BR Smith. "Aspirin does not inhibit adenosine diphosphate-induced platelet alpha- granule release." Blood 82, no. 2 (1993): 505–12. http://dx.doi.org/10.1182/blood.v82.2.505.bloodjournal822505.

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The involvement of metabolites of arachidonic acid in platelet-dense granule secretion and secondary platelet-platelet interactions is well characterized. However, their role in heterotypic interactions dependent on alpha-granule secretion is less well understood. Using platelet-surface expression of P-selectin as a marker of alpha-granule secretion, we have shown that: (1) aspirin treatment of platelets at doses that block dense granule secretion does not inhibit alpha-granule secretion to adenosine diphosphate (ADP); (2) synergism between epinephrine and ADP in the induction of P-selectin ex

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Pedersen, Oliver Buchhave, Anne-Mette Hvas, Hans Beier Ommen, Steen Dalby Kristensen, and Erik Lerkevang Grove. "Lower Antiplatelet Effect of Aspirin in Essential Thrombocythemia than in Coronary Artery Disease." TH Open 05, no. 03 (2021): e230-e238. http://dx.doi.org/10.1055/s-0041-1731309.

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Abstract Background Patients with essential thrombocythemia (ET) and coronary artery disease (CAD) have increased risk of thromboembolic complications. In addition, a reduced antiplatelet effect of aspirin has been demonstrated in both patient groups. As ET is a platelet disorder, platelets may be more important for the thromboembolic risk in ET than in CAD. We aimed to investigate the antiplatelet effect of aspirin and platelet turnover in ET versus CAD patients. Methods We included 48 ET patients and an age-matched group of 48 CAD patients. The effect of aspirin was evaluated by thromboxane

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Armstrong, Paul C., Thomas Hoefer, Rebecca B. Knowles, et al. "Newly Formed Reticulated Platelets Undermine Pharmacokinetically Short-Lived Antiplatelet Therapies." Arteriosclerosis, Thrombosis, and Vascular Biology 37, no. 5 (2017): 949–56. http://dx.doi.org/10.1161/atvbaha.116.308763.

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Objective— Aspirin together with thienopyridine P2Y 12 inhibitors, commonly clopidogrel, is a cornerstone of antiplatelet therapy. However, many patients receiving this therapy display high on-treatment platelet reactivity, which is a major therapeutic hurdle to the prevention of recurrent thrombotic events. The emergence of uninhibited platelets after thrombopoiesis has been proposed as a contributing factor to high on-treatment platelet reactivity. Here, we investigate the influences of platelet turnover on platelet aggregation in the face of different dual-antiplatelet therapy strategies. A

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Lim, Eric, Martin Goddard, Sarah Bellm, et al. "Biological efficacy of low against medium dose aspirin regimen after coronary surgery: Analysis of platelet function." Thrombosis and Haemostasis 95, no. 03 (2006): 476–82. http://dx.doi.org/10.1160/th05-10-0649.

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SummaryThe failure of aspirin to inhibit platelet function has been documented in patients undergoing coronary artery bypass graft (CABG) surgery, but the causes of “aspirin-resistance” remain uncertain. The aim of this study was to investigate the efficacy of aspirin in patients undergoing CABG surgery receiving either 100 mg or 325 mg of oral aspirin for 5-days.Platelet function was tested the day before surgery and on day+1 and day+5, and evaluated by changes in collagen-induced thromboxane-A2 (TxA2) release and platelet aggregation following stimulation with collagen, ADP and epinephrine.

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Rottenstreich, Amihai, Roger Vaughan, and Barry S. Coller. "286 Genetic, laboratory and clinical factors associated with low-dose aspirin failure in the prevention of preeclampsia." Journal of Clinical and Translational Science 7, s1 (2023): 86. http://dx.doi.org/10.1017/cts.2023.342.

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OBJECTIVES/GOALS: Low-dose aspirin is an established treatment to prevent preeclampsia, a leading cause of maternal and perinatal complications. Nevertheless, aspirin failure is not uncommon. We are investigating whether a gain-of-function genetic polymorphism in a platelet thrombin receptor is associated with aspirin failure in the prevention of preeclampsia. METHODS/STUDY POPULATION: Women who had preeclampsia in an initial pregnancy who then received low-dose aspirin in a subsequent pregnancy will be evaluated. We will compare between women who developed preeclampsia despite aspirin (aspiri

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Brambilla, Marta, Alessandro Parolari, Marina Camera, et al. "Effect of two doses of aspirin on thromboxane biosynthesis and platelet function in patients undergoing coronary surgery." Thrombosis and Haemostasis 103, no. 03 (2010): 516–24. http://dx.doi.org/10.1160/th09-07-0470.

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SummaryEarly post-operative aspirin improves survival in patients undergoing coronary artery bypass graft (CABG). However, most patients do not benefit of aspirin after CABG, still remaining at risk of thrombotic events due to insufficient platelet inhibition, specifically via the thromboxane (TX) pathway. We evaluated the effect of two aspirin doses (100 or 325 mg daily, enteric coated formulations) on platelet function and TX biosynthesis in patients after CABG and assessed whether the incidence of residual platelet reactivity could be reduced by the higher dose. Fifty-six patients undergoin

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Gerritsen, Wim, Fred Haas, Johannes Kelder, Freek Verheugt, H. W. Plokker, and Jurriën M. Berg. "Pretreatment with Oral Anticoagulants Decreases Platelet Activation in Patients Before and After Percutaneous Coronary Intervention." Thrombosis and Haemostasis 88, no. 12 (2002): 924–30. http://dx.doi.org/10.1055/s-0037-1613335.

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SummaryPlatelet activation plays a major role in acute vessel closure after coronary angioplasty. In the randomized Balloon Angioplasty and Anticoagulation Study (BAAS), pretreatment with oral anticoagulants in addition to aspirin resulted in a 47% reduction of acute complications as compared with aspirin alone. This result may suggest a direct effect of oral anticoagulants on platelet activation.Patients were randomized to aspirin alone (group A, n = 26) or to aspirin plus oral anticoagulants started one week before angioplasty (group B, n = 26). Platelet response tests were performed 1 hour

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Shen, Jian, Fei Yang, Yujun Shen, Ying Yu, Timothy J. Stalker, and Li Zhu. "Thromboxane A2 Signaling Regulates Heterogeneous Platelet Activation Following Laser-Induced Injury In Mouse Cremaster Arterioles." Blood 122, no. 21 (2013): 1055. http://dx.doi.org/10.1182/blood.v122.21.1055.1055.

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Abstract Background A recent study demonstrated that platelet accumulation following vascular injury in vivo is hierarchically organized resulting in a structure comprised of a core of fully-activated platelets that is overlaid with an unstable shell of less activated platelets (Stalker et al, Blood, 2013). This structure results from different elements of the platelet signaling network giving rise to regions that differ in platelet activation state, packing density, and stability. It was thus proposed that regional differences in platelet activation reflect regional differences in the distrib

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Valles, J., MT Santos, J. Aznar, et al. "Erythrocytes metabolically enhance collagen-induced platelet responsiveness via increased thromboxane production, adenosine diphosphate release, and recruitment." Blood 78, no. 1 (1991): 154–62. http://dx.doi.org/10.1182/blood.v78.1.154.154.

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Abstract Erythrocytes promoted platelet reactivity in a plasma medium, as demonstrated in an in vitro system that independently evaluated the biochemistry of platelet activation and recruitment. The prothrombotic erythrocyte effects were metabolically regulated, as evidenced by lack of activity of ATP-depleted or glutaraldehyde-fixed erythrocytes. They occurred in the absence of cell lysis as verified by lactate dehydrogenase assays, and had an absolute requirement for platelet activation. The presence of erythrocytes induced a twofold increase in platelet thromboxane B2 (TXB2) synthesis upon

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Valles, J., MT Santos, J. Aznar, et al. "Erythrocytes metabolically enhance collagen-induced platelet responsiveness via increased thromboxane production, adenosine diphosphate release, and recruitment." Blood 78, no. 1 (1991): 154–62. http://dx.doi.org/10.1182/blood.v78.1.154.bloodjournal781154.

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Erythrocytes promoted platelet reactivity in a plasma medium, as demonstrated in an in vitro system that independently evaluated the biochemistry of platelet activation and recruitment. The prothrombotic erythrocyte effects were metabolically regulated, as evidenced by lack of activity of ATP-depleted or glutaraldehyde-fixed erythrocytes. They occurred in the absence of cell lysis as verified by lactate dehydrogenase assays, and had an absolute requirement for platelet activation. The presence of erythrocytes induced a twofold increase in platelet thromboxane B2 (TXB2) synthesis upon collagen

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Chen, Chuan-Mu, Hsiao-Ching Lu, Yu-Tang Tung, and Wei Chen. "Antiplatelet Therapy for Acute Respiratory Distress Syndrome." Biomedicines 8, no. 7 (2020): 230. http://dx.doi.org/10.3390/biomedicines8070230.

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Acute respiratory distress syndrome (ARDS) is a common and devastating syndrome that contributes to serious morbidities and mortality in critically ill patients. No known pharmacologic therapy is beneficial in the treatment of ARDS, and the only effective management is through a protective lung strategy. Platelets play a crucial role in the pathogenesis of ARDS, and antiplatelet therapy may be a potential medication for ARDS. In this review, we introduce the overall pathogenesis of ARDS, and then focus on platelet-related mechanisms underlying the development of ARDS, including platelet adhesi

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Tao, Derrick L., Samuel Tassi Yunga, Craig D. Williams, and Owen J. T. McCarty. "Aspirin and antiplatelet treatments in cancer." Blood 137, no. 23 (2021): 3201–11. http://dx.doi.org/10.1182/blood.2019003977.

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Abstract Platelets have been hypothesized to promote certain neoplastic malignancies; however, antiplatelet drugs are still not part of routine pharmacological cancer prevention and treatment protocols. Paracrine interactions between platelets and cancer cells have been implicated in potentiating the dissemination, survival within the circulation, and extravasation of cancer cells at distant sites of metastasis. Signals from platelets have also been suggested to confer epigenetic alterations, including upregulating oncoproteins in circulating tumor cells, and secretion of potent growth factors

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Laidlaw, Tanya M., Molly S. Kidder, Neil Bhattacharyya, et al. "Cysteinyl leukotriene overproduction in aspirin-exacerbated respiratory disease is driven by platelet-adherent leukocytes." Blood 119, no. 16 (2012): 3790–98. http://dx.doi.org/10.1182/blood-2011-10-384826.

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Abstract Cysteinyl leukotriene (cysLT) overproduction is a hallmark of aspirin-exacerbated respiratory disease (AERD), but its mechanism is poorly understood. Because adherent platelets can convert the leukocyte-derived precursor leukotriene (LT)A4 to LTC4, the parent cysLT, through the terminal enzyme LTC4 synthase, we investigated the contribution of platelet-dependent transcellular cysLT production in AERD. Nasal polyps from subjects with AERD contained many extravascular platelets that colocalized with leukocytes, and the percentages of circulating neutrophils, eosinophils, and monocytes w

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Vallés, Juana, M. Teresa Santos, Justo Aznar та ін. "Platelet-erythrocyte interactions enhance αIIbβ3 integrin receptor activation and P-selectin expression during platelet recruitment: down-regulation by aspirin ex vivo". Blood 99, № 11 (2002): 3978–84. http://dx.doi.org/10.1182/blood.v99.11.3978.

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Activated platelets release biologically active compounds, which then recruit additional platelets into an evolving thrombus. We studied activation of αIIbβ3 and exposure of P-selectin on platelets recruited by releasates obtained from collagen-treated platelets and evaluated modifications in prothrombotic effects of releasates induced by platelet-erythrocyte interactions and aspirin treatment. Releasates from collagen-stimulated platelets induced αIIbβ3 activation and P-selectin exposure (monitored by flow cytometry using fluorescein isothiocyanate–PAC-1 and phycoerythrin-CD62 antibodies). Th

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Giannini, Silvia, Emanuela Falcinelli, Loredana Bury, et al. "Interaction with damaged vessel wall in vivo in humans induces platelets to express CD40L resulting in endothelial activation with no effect of aspirin intake." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 6 (2011): H2072—H2079. http://dx.doi.org/10.1152/ajpheart.00467.2010.

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Activated platelets express CD40L on their plasma membrane and release the soluble fragment sCD40L. The interaction between platelet surface CD40L and endothelial cell CD40 leads to the activation of endothelium contributing to atherothrombosis. Few studies have directly demonstrated an increased expression of platelet CD40L in conditions of in vivo platelet activation in humans, and no data are available on its relevance for endothelial activation. We aimed to assess whether platelets activated in vivo at a localized site of vascular injury in humans express CD40L and release sCD40L, whether

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Penz, Sandra, Armin Reininger, Orsolya Toth, Hans Deckmyn, Richard Brandi та Wolfgang Siess. "Glycoprotein Ibα inhibition and ADP receptor antagonists, but not aspirin, reduce platelet thrombus formation in flowing blood exposed to atherosclerotic plaques". Thrombosis and Haemostasis 97, № 03 (2007): 435–43. http://dx.doi.org/10.1160/th06-07-0415.

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SummaryAnti-platelet drugs are used to prevent intra-arterial thrombus formation after rupture of atherosclerotic plaques. Until now, the inhibitory effect of present and future anti-platelet drugs such as aspirin, ADP receptor P2Y1/P2Y12 antagonists and glycoprotein (GP) Ibα inhibitors on the interaction of platelets with human plaques is not known. To study those effects we obtained human atherosclerotic plaques by surgical endarterectomy. Plaques induced maximal platelet aggregation in hirudinized platelet-rich plasma (PRP) and blood that was effectively inhibited by aspirin, the P2Y1 antag

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Scazziota, Alejandra, Jorge Rouvier, Claudio Gonzalez, and Raul Altman. "Effect of Sodium Arachidonate on Thrombin Generation through Platelet Activation – Inhibitory Effect of Aspirin." Thrombosis and Haemostasis 84, no. 12 (2000): 1109–12. http://dx.doi.org/10.1055/s-0037-1614178.

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Summary Background. Sodium arachidonate was used in this study to determine its capacity to generate thrombin through platelet activation. Whether aspirin prevent this effect was also investigated. Methods and Results. Seventeen healthy volunteers without and after 160 mg/day aspirin intake for 3-5 days were studied. Lag-time and TG at basal condition and after platelet stimulation by sodium arachidonate (AA) were measured in normal non-aspirinated as well as “in vivo” aspirinated platelet rich plasma. (PRP). The lag-time was statistically significant shorter in non-aspirinated PRP activated w

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McCulloch, R. K., J. Summers, R. Vandongen, and I. L. Rouse. "Role of Thromboxane A2 as a Mediator of Platelet-Activating-Factor-Induced Aggregation of Human Platelets." Clinical Science 77, no. 1 (1989): 99–103. http://dx.doi.org/10.1042/cs0770099.

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1. At present it is unclear whether platelet-activating-factor (PAF)-induced aggregation is mediated by thromboxane. To obtain further information about this event we have compared the affects of aspirin on platelet aggregation and secretion induced by PAF and collagen. 2. Collagen and PAF induced aggregation and secretion in human platelets in a dose-related manner. 3. Aspirin inhibited the magnitude of both platelet aggregation and secretion induced by PAF and collagen, but the degree of inhibition was much greater for collagen. 4. Aspirin strongly inhibited the aggregation rate of collagen-

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Howard, Patricia A. "Aspirin Resistance." Annals of Pharmacotherapy 36, no. 10 (2002): 1620–24. http://dx.doi.org/10.1345/aph.1c013.

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OBJECTIVE: To review the literature addressing the problem of aspirin resistance in patients with vascular disease. DATA SOURCES: A MEDLINE search (1966–February 2002) was performed. Key search terms included aspirin, resistance, resistant, failure, tolerance, and nonresponder. English-language studies were identified as well as pertinent references from these articles. DATA SYNTHESIS: Aspirin resistance has been reported in patients with cardiovascular, cerebrovascular, and peripheral vascular disease. Because of differences in the definition of resistance, variations in detection methods, an

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Crescente, Marilena, Gisela Jessen, Stefania Momi, et al. "Interactions of gallic acid, resveratrol, quercetin and aspirin at the platelet cyclooxygenase-1 level Functional and modelling studies." Thrombosis and Haemostasis 102, no. 08 (2009): 336–46. http://dx.doi.org/10.1160/th09-01-0057.

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SummaryWhile resveratrol and quercetin possess antiplatelet activity, little is known on the effect of gallic acid on platelets.We studied the interactions of these three different polyphenols among themselves and with aspirin, at the level of platelet cyclooxygenase-1 (COX-1). Both functional (in vitro and in vivo) and molecular modelling approaches were used. All three polyphenols showed comparable antioxidant activity (arachidonic acid [AA]-induced intraplatelet ROS production); however, resveratrol and quercetin, but not gallic acid, inhibited AA-induced platelet aggregation. Gallic acid,

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