Platelet aggregability was studied in 18 healthy volunteers during mental stress (a colour word test; CWT) and low- and high-dose adrenaline infusions using an ex vivo technique (filtragometry) and conventional in vitro aggregometry. CWT and high-dose adrenaline (3.4 nmol l-1 in plasma) shortened filtragometry readings, suggesting increased platelet aggregability in vivo. Low-dose adrenaline had no effect despite higher adrenaline levels in plasma (0.9 nmol l-1) than during CWT (0.4 nmol l-1). Platelet sensitivity to ADP in vitro was reduced following CWT and further reduced following adrenaline infusions. In vitro, adrenaline (50 nmol l-1) had little effect on platelet aggregation per se, but enhanced aggregability evoked by ADP (at ED50). Adrenaline potentiation of ADP-induced aggregation was enhanced after CWT, but was not related to filtragometry responsiveness to stress in vivo. Serum LDL-cholesterol levels were inversely correlated to filtragometry readings at rest, suggesting an adverse influence on platelet aggregability in vivo. HDL-cholesterol levels were inversely correlated to platelet sensitivity to ADP in vitro, suggesting a positive influence. Thus, sympatho-adrenal activation enhances platelet aggregability in vivo (as assessed by ex vivo filtragometry), but adrenaline alone cannot explain the pro-aggregatory effect of mental stress. Serum lipoprotein alterations associated with increased risk for atherosclerosis seem to enhance platelet aggregability. The conventional in vitro technique may poorly reflect platelet aggregability in vivo.
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http://dx.doi.org/10.1111/j.1365-2362.1990.tb01876.x | DOI Listing |
Anal Chem
January 2025
Department of Anesthesiology, Tokyo Medical and Dental University, Graduate School of Medical and Dental Sciences, 1-5-45 Yushima, Bunkyo-ku 113-8510, Tokyo, Japan.
The hemostatic function of platelets is complementary to blood coagulation. However, traditional platelet function tests have primarily focused on measuring platelet aggregation, reducing their clinical effectiveness for antiplatelet drug monitoring. To address this limitation, we propose a new test principle that evaluates platelet function and the effects of antiplatelet drugs through blood coagulation reactions.
View Article and Find Full Text PDFOral Maxillofac Surg
January 2025
Department of Developmental and Surgical Sciences, Division of Periodontology, School of Dentistry, University of Minnesota, 515 Delaware Street SE, Minneapolis, MN, 55455, USA.
Purpose: This large-scale retrospective study aimed to examine the long-term effect of antiplatelet and anticoagulant medications intake on dental implant treatment outcome.
Materials And Methods: This study retrospectively examined data from patients who underwent dental implant procedures at several university dental clinics within the BigMouth network between 2011 and 2022. Patients' characteristics including age, gender, ethnicity, race, tobacco use, systemic medical conditions and intake of antiplatelets and anticoagulants were analyzed.
Hernia
January 2025
Department of Minimally Invasive Surgery, National University Hospital, Bukit Timah, Singapore.
Background: Given the increasing prevalence of antiplatelet agent use and the lack of high-quality evidence, the CAPTAIN trial aimed to investigate the safety and provide recommendations on continuing acetylsalicylic acid perioperatively in patients undergoing elective laparoscopic totally extraperitoneal inguinal hernia repair (LIHR).
Methods: The CAPTAIN trial was a multicentre, surgeon blind, randomized controlled trial conducted from April 2016 to April 2023. Patients undergoing LIHR were eligible for inclusion.
Res Pract Thromb Haemost
January 2025
Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Background: Reduced effect of antiplatelet therapy has been reported in patients with ST-segment elevation myocardial infarction (STEMI). This could partly be explained by an increase of highly reactive immature platelets.
Objectives: To investigate changes in platelet maturity and reactivity after acute STEMI.
Se Pu
February 2025
Shanghai-MOST Key Laboratory of Health and Disease Genomics, NHC Key Lab of Reproduction Regulation, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Shanghai 200237, China.
Thromboxane A (TXA), a prothrombotic factor that induces platelet aggregation and thrombosis, acts as a vasoconstrictor by activating TXA receptors (TP receptors). TXA is extremely unstable and metabolizes into three major metabolites: 2,3-dinor thromboxane B (2,3-dinor-TXB), 11-dehydro TXB(11-dh-TXB), and 11-dehydro-2,3-dinor TXB(11-dh-2,3-dinor-TXB). 8-Iso-prostaglandin F(8-iso-PGF), a prostaglandin-like compound widely considered the best biomarker of oxidative stress, can also activate TP receptors.
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