ArticleJournal of thrombosis and haemostasis : JTH2022
Importance of catecholamine signaling in the development of platelet exhaustion after traumatic injury.
Article in Journal of thrombosis and haemostasis : JTH, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Platelets and inflammation-insights from platelet non-coding RNA content and release in the Bruneck study and the PACMAN-AMI trial.Cardiovascular research · 2025Trial
- Hallmarks of the multidimensional immune response to trauma in humans.Nature immunology · 2026Review
- A rare initial presentation of giant pheochromocytoma: a case report of acute pulmonary embolism complicated by catecholamine-induced cardiomyopathy.Frontiers in oncology · 2026Article
- Catecholamines in sepsis: pharmacological insights and clinical applications-a narrative review.Journal of anesthesia, analgesia and critical care · 2025Review
- Beyond the heart: a review exploring non-cardiovascular effects of vasoactive agents.Frontiers in pharmacology · 2025Review
- High-Dimensional Single-Cell Mass Cytometry Demonstrates Differential Platelet Functional Phenotypes in Infants With Congenital Heart Disease.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Traumatic brain injury: Advances in coagulopathy (Review).Biomedical reports · 2024Review
- Highly Efficient Hemostatic Cross-Linked Polyacrylate Polymer Dressings for Immediate Hemostasis.Polymers · 2024Article
- The role of platelets in sepsis: A review.Biomolecules & biomedicine · 2024Review
- Effects of the circulating environment of COVID-19 on platelet and neutrophil behavior.Frontiers in immunology · 2023Article
- Activation of Most Toll-Like Receptors in Whole Human Blood Attenuates Platelet Deposition on Collagen under Flow.Journal of immunology research · 2023Article
- Tranexamic acid for the prevention of postpartum bleeding in women with anaemia: Statistical analysis plan for the WOMAN-2 trial: an international, randomised, placebo-controlled trial.Gates open research · 2023Article
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10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundImpaired ex vivo platelet aggregation is common in trauma patients. The mechanisms driving these impairments remain incompletely understood, but functional platelet exhaustion due to excessive in vivo activation is implicated. Given platelet adrenoreceptors and known catecholamine surges after injury, impaired ex vivo platelet aggregation in trauma patients may be linked to catecholamine-induced functional platelet exhaustion.
objectiveTo determine the relationship of catecholamines with platelet-dependent hemostasis after injury and to model catecholamine-induced functional platelet exhaustion in healthy donor platelets. PATIENTS/
methodsWhole blood was collected from 67 trauma patients as part of a prospective cohort study. Platelet aggregometry and rotational thromboelastometry were performed, and plasma epinephrine (EPI) and norepinephrine (NE) concentrations were measured. The effect of catecholamines on healthy donor platelets was examined in a microfluidic model, with platelet aggregometry, and by flow cytometry examining surface markers of platelet activation.
resultsIn trauma patients, EPI and NE were associated with impaired platelet aggregation (both p < 0.05), and EPI was additionally associated with decreased viscoelastic clot strength, increased fibrinolysis, and mortality (all p < 0.05). In healthy donors, short duration incubation with EPI enhanced platelet aggregation, platelet adhesion under flow, and increased glycoprotein IIb/IIIa activation, while weaker effects were observed with NE. Compared with short incubation, longer incubation with EPI resulted in decreased platelet adhesion, platelet aggregation, and surface expression of glycoprotein IIb/IIIa.
conclusionsThese findings suggest sympathoadrenal activation in trauma patients contributes to impaired ex vivo platelet aggregation, which mechanistically may be explained by a functionally exhausted platelet phenotype under prolonged exposure to high plasma catecholamine levels.
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