Probing microstructural differences that manifest in human blood after taking aspirin using thixo-elasto-visco-plastic modeling and series of physical processes

Matthew Armstrong,Chi Nguyen,Andre Pincot,Lam Nguyen,Erin Milner,Trevor Corrigan,Dorian Bailey,Thomas Brown,Kevin O’Donovan

doi:10.1063/5.0074608

Abstract

Although prophylactic use of low dosage acetylsalicylic acid (aspirin) to inhibit the effects of platelet aggregation is common, a few, if any, rheological studies validating the change in the physical and mechanical properties of human blood post-aspirin administration have been reported. Recent work modeling the rheological behavior of thixo-elasto-visco-plastic materials, such as human blood, indicates that they have all the hallmark features of a complex material, including shear-thinning, viscoelasticity, yield stress, and thixotropy. Using human blood rheological data collected on a Discovery Hybrid Rheometer, before and after a 14-day protocol of once daily 81 mg aspirin tablet, we compare the mechanical properties with the recently published enhanced thixotropic modified Horner–Armstrong–Wagner–Beris thixo-elasto-visco-plastic model and sequence of physical processes. We do so to highlight the subtle shift in mechanical properties in terms of the “liquid-like” and “solid-like” nature of blood. We will show both before and after parametric analysis, profile, and comparison, as well as the before and after aspirin elastic and viscous properties of the human blood.

Highlights

The use of aspirin can substantially lengthen bleeding duration, inhibiting the production and subsequent aggregation of platelet thromboxane A2 (TXA2) via the acetylation of serine located near the active site of the cyclooxygenase-1 enzyme (COX-1)
Platelet aggregation caused by TXA2-independent pathways, such as thrombin formation, remains unchanged during aspirin administration
In accordance with procedures approved by the United States Military Academy’s Institutional Review Board (RHCA19037_918567), experimental blood samples were drawn from the antecubital veins of the seated donors after tourniquet application following 14 consecutive days of daily 81 mg aspirin administration

Summary

Introduction

Due to its ability to reduce blood viscosity and preempt coagulation by platelet aggregation, aspirin is one of the world’s most widely used drugs for pain suppression applications and the treatment of cardiovascular or arterial thrombotic disorders. Despite its utility in improving vascular health, the anticoagulant properties of aspirin have been noted to increase the severity and occurrence of major bleeding events. The long history of salicylic acid as an antipyretic, anti-inflammatory, and analgesic agent made it the principal precursor of aspirin. Taken orally, aspirin is rapidly absorbed and partially hydrolyzed into salicylate upon first pass through the liver, achieving a maximum concentration (Cmax) in plasma within 30 min. Bloodstream platelet aggregation is aspirin dose dependent and related to the anti-thrombus mechanism of action in the coronary and vascular circulation systems.The use of aspirin can substantially lengthen bleeding duration, inhibiting the production and subsequent aggregation of platelet thromboxane A2 (TXA2) via the acetylation of serine located near the active site of the cyclooxygenase-1 enzyme (COX-1). Regular aspirin administration irreversibly inhibits COX-1 dependent TXA2 formation, thereby interfering with platelet reactivity and functioning as a positive-feedback mediator during platelet activation. After the initial production of the platelets, platelet secretion and aggregation can be hampered for as long as 12 days because platelets cannot produce new proteins. Platelet aggregation caused by TXA2-independent pathways, such as thrombin formation, remains unchanged during aspirin administration.. Despite its utility in improving vascular health, the anticoagulant properties of aspirin have been noted to increase the severity and occurrence of major bleeding events.. The long history of salicylic acid as an antipyretic, anti-inflammatory, and analgesic agent made it the principal precursor of aspirin.. Bloodstream platelet aggregation is aspirin dose dependent and related to the anti-thrombus mechanism of action in the coronary and vascular circulation systems. The use of aspirin can substantially lengthen bleeding duration, inhibiting the production and subsequent aggregation of platelet thromboxane A2 (TXA2) via the acetylation of serine located near the active site of the cyclooxygenase-1 enzyme (COX-1).. Regular aspirin administration irreversibly inhibits COX-1 dependent TXA2 formation, thereby interfering with platelet reactivity and functioning as a positive-feedback mediator during platelet activation.. Platelet aggregation caused by TXA2-independent pathways, such as thrombin formation, remains unchanged during aspirin administration.

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Results

Conclusion