Platelet-driven contraction enlarges accessible space in layered fibrin networks without uniformly accelerating particle escape

Abstract

Platelet traction contracts fibrin networks, yet whether contraction promotes or hinders the escape of suspended particles is unclear. We coupled an overdamped Langevin model of platelet--fibrin mechanics to Brownian transport of finite-size tracers through frozen network states. Nine mechanical replicas were evolved at four filopodial traction baselines (0--8.8\,nN), stacked into 5-$μ$m-thick domains of 50 layers and probed at 0--15\,s with 0.5-$μ$m tracers (29,952 trajectories, 100\,s observation). Benchmarked against experimental clot-contraction kinetics, the simulated contraction is post-lag, within one order of magnitude of experimental rates and corresponds to the onset of the contraction phase. Relative to the matched zero-baseline control, every active-baseline state showed greater projected contraction and a larger tracer-accessible volume ($+9.3\%$ to $+27.6\%$; exact sign test $p=0.0039$ per condition). At 15\,s, mean survival at 100\,s fell from 27.3\% to 14.3\% and the restricted mean exit time from 56.5 to 44.0\,s between the lowest and highest baseline, and all nine replicas shortened residence at 8.8\,nN. At lower baselines, responses differed among replicas, and nearly all retained tracers with a classified start were connected to an exit. Contraction therefore enlarges accessible space without uniformly accelerating escape, separating geometric accommodation from transport kinetics.