After wounding, there is transient vasoconstriction mediated by catecholamines, thromboxane, and prostaglandin F2 (PGF2a). This period of vasoconstriction lasts for only five to ten minutes. Once a clot has been formed and active bleeding has stopped, vasodilatation occurs in an around the wound. Vasodilatation increases local blood flow to the wounded area, supplying the cells and substrate necessary for fuher wound repair. The vascular endothelial cells also deform, increasing vascular permeability. The vasodilatation and increased endothelial permeability is mediated by histamine, PGE2, and prostacyclin as well as growth factor VEGF (vascular endothelial cell growth factor). These vasodilatory substances are released by injured endothelial cells and mast cells and enhance the egress of cells and substrate into the wound and tissue.