# Red cell microparticles produced using high-pressure extrusion enhance both primary and secondary hemostasis

## TL;DR

Red blood cell microparticles improve both primary and secondary blood clotting processes, suggesting potential as a safer treatment for excessive bleeding.

## Contribution

This study reveals that red cell microparticles enhance both primary and secondary hemostasis, providing new insights into their mechanism of action.

## Key findings

- RMPs significantly increased collagen-induced platelet aggregation.
- RMPs decreased clotting times in plasma deficient in factors VII, VIII, IX, and XI.
- RMPs had no significant effect on plasma deficient in factor XII.

## Abstract

Current therapies to treat excessive bleeding are associated with significant complications, which may outweigh their benefits. Red blood cell-derived microparticles (RMPs) are a promising hemostatic agent. Previous studies demonstrated that they reduce bleeding in animal models, correct coagulation defects in patient blood, and have an excellent safety profile. However, their exact mechanism of action is not known. We investigated the potential role of RMPs on primary and secondary hemostasis.

To evaluate the effects of RMPs, prepared using high-pressure extrusion, on primary hemostasis, we employed platelet aggregometry with platelet inhibitors, eptifibatide, and ticagrelor, with and without RMPs. To evaluate their effects on secondary hemostasis, we employed thromboelastography with plasma deficient in factors VII, VIII, IX, XI, and XII with and without RMPs.

We found that RMPs significantly increased collagen-induced platelet aggregation. However, there were no significant differences with and without RMP in the presence of the platelet inhibitors, indicating that RMPs may work through these receptors, either directly or indirectly. For secondary hemostasis, RMPs significantly decreased clotting times for plasma deficient in factors VII, VIII, IX, and XI but not in XII.

Our results indicate that RMPs enhance primary hemostasis and both pathways of secondary hemostasis.

The online version contains supplementary material available at 10.1007/s43440-024-00688-0.