Key result
Transient high shear stress effectively activates platelets and increases activity markers versus low shear stress.
Why the study?
Platelet adhesion and aggregation behavior at nonphysiological post-stenosis, along with its affecting factors, are not fully understood.
Transient high shear stress, such as that found post-stenosis, significantly activates platelets and promotes aggregation, highlighting biomechanical factors in thrombosis.
Answers are grounded in this paper and cite their sources.
Alerts to thrombotic risk in high-shear devices; leaves open clinical translation of 46-ms platelet activation.
BACKGROUND: When nonphysiological stenosis occurs, the transient high shear stress formed in vessels increases the risk of thrombosis and is a potential factor for cardiovascular diseases. But the platelet adhesion and aggregation behavior at nonphysiological post-stenosis and its affecting factors are not fully understood yet. METHODS: In this experiment, platelet aggregation on collagen and fibrinogen at different shear stresses and different hematocrits were observed by microfluidic technology. Platelet activation (P-selectin, glycoprotein IIb/IIIa) and monocyte-platelet aggregate (MPA) levels under different shear stresses were analyzed by flow cytometry. RESULTS: On fibrinogen, platelets aggregate more at higher shear stress conditions. While on collagen, it becomes more difficult for platelets to form stable aggregation at higher shear stress conditions. If platelets adhere initially at low shear stress, stable platelet aggregation can be formed at subsequent high shear stress. Moreover, when the shear stress increases, platelet activity markers (P-selectin, glycoprotein IIb/IIIa and MPAs) increase significantly. Hematocrit affects the degree of platelet aggregation, and the influence of hematocrit is obvious at high shear stress. CONCLUSION: Transient high shear stress (46 ms) can effectively activate platelets. Platelet aggregation behavior was different for coated fibrinogen and collagen protein. Stable platelet adhesion at post-stenosis is more dependent on fibrinogen and platelet aggregation is stable on both fibrinogen and collagen. Hematocrit can significantly affect the formation of platelet aggregation.
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Gao et al. (2023) studied Thrombosis risk. Transient high shear stress vs. Low shear stress was evaluated on Platelet activation, adhesion, and aggregation. Transient high shear stress (46 ms) effectively activated platelets and significantly increased platelet activity markers including P-selectin, glycoprotein IIb/IIIa, and monocyte-platelet aggregates.
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