Figure 4.

Traveling wave propagation is stopped by thrombomodulin: possible implications for confining a hemostatic plug to the wound. (A) Spatiotemporally resolved distribution of thrombin in normal plasma supplemented with different concentrations of thrombomodulin, as indicated in the panels. Plasma is supplemented with 10 μM phospholipids. Activation is with 4 pmol TF/m². A typical experiment (out of n = 5) is shown. (B) Clot size (main plot), spatial velocity (left inset), and thrombin peak amplitude (right inset) as functions of time for different thrombomodulin concentrations. (C) Hypothetical function of the traveling wave of thrombin in vivo. In a sufficiently large wound, it is necessary to turn all of the blood into a gel, and to spread the clot from the TF-containing injury site into the bulk of the blood. This task is possible, because thrombin propagation can be self-sustained due to factor XI feedback activation, which explains the bleeding upon large injuries in hemophilia C. Abundant thrombomodulin in the healthy blood vessel endothelium prevents the traveling wave from entering the healthy vasculature.