Background The cremaster arteriole laser‐induced injury model is a powerful technique with
which to investigate the molecular mechanisms that drive thrombus formation. This model is
capable of direct visualization and quantification of accumulation of thrombus constituents,
including both platelets and fibrin. However, a large degree of variability in platelet
accumulation and fibrin formation is observed between thrombi. Strategies to understand
this variability will enhance performance and standardization of the model. We determined …