AI Article Synopsis
- Trauma patients often exhibit impaired platelet aggregation, which may be tied to functional exhaustion from heightened catecholamine levels like epinephrine and norepinephrine after injury.
- A study involving 67 trauma patients showed that increased catecholamines were linked to reduced platelet function and clots, with epinephrine being especially impactful on mortality and clot strength.
- In healthy donors, short-term exposure to epinephrine boosted platelet activity, but prolonged exposure led to a drop in platelet adhesion and aggregation, suggesting that time and concentration of catecholamines play a crucial role in platelet function.
Article Abstract
Background: Impaired 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.
Objective: To determine the relationship of catecholamines with platelet-dependent hemostasis after injury and to model catecholamine-induced functional platelet exhaustion in healthy donor platelets.
Patients/methods: Whole 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.
Results: In 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.
Conclusions: These 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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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10450647 | PMC |
| http://dx.doi.org/10.1111/jth.15763 | DOI Listing |
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