Contraction of blood clots occurs during hemostasis and hemorrhagic shock to promote closure of lacerations.

Hemorrhage is a leading cause of mortality in humans, responsible for approximately two million deaths annually worldwide. The contraction of blood clots is a robust process that occurs intravascularly to reduce the size of pathological thrombi. However, it is not clear if clot contraction contributes to hemostasis. Here we show that blood clots in laceration wounds contract, and the forces can decrease the size of wounds by up to 80%. Clots contracted after penetrating injuries in swine, as revealed by scanning electron microscopy. Contraction was robust throughout hemorrhagic shock in two swine models, with ex vivo clots becoming 20-40% of their initial volume (60-80% contraction) at sustained rates of ∼1.5% of clot volume min-1. In two models of laceration, one using a synthetic gel and the other using ex vivo lacerated livers, contraction decreased the size of wounds in a platelet-dependent response, generating forces up to approximately 0.5 N. A ten-fold increase in platelet count increased the closure by ∼22%. A mechanics-based computational model representing the clot as a tunable biomaterial composed of fibrin fibers and platelet motors replicated and confirmed this phenomenon. Thus, platelet-driven clot contraction is an important component of the hemostatic response to severe injury, and contraction is a tunable process that may be useful for improving biomaterials for hemostasis.