The interaction of platelets with the extracellular matrix (i.e., collagen) has been the subject of intensive research in the past 25 years. With today's knowledge it is possible to explain why blood loss is minimal in cases of arterial rupture. As discussed earlier, a direct interaction of platelets with collagen was suspected for cellular thrombogenesis in arterial injuries. The first step in this interaction is a loose adhesion of platelets onto mature collagen with activation of the platelets. This is followed by aggregation and activation of the platelets through adhesins, which interact with special glycoproteins of the platelet's surface. At the same time, fibrinogenesis is started and facilitated by expression of platelet-factor 3 from the membrane surface of the platelet, so the production of thrombin is acclerated. The activation of platelets induces mobilization of calcium from the dense tubular system, which is needed for almost all reactions in arterial thrombogenesis. Exogene and platelet-endogene factors are responsible for the platelet activation. The further activation of platelets is maintained by thromboxane A2 and thrombin. The regulation of platelet aggregation is controlled by cAMP and prostacyclin. These well-documented findings are the reason for the very rapid arterial thrombogenesis in cases of arterial rupture combined with a special "fingertrap mechanism" of the scissorlike structure of the adventitia. Therefore, severe hemorrhage is prevented. Even in microvascular lesions the platelet-collagen interaction will be found, so this mechanism must also be considered in the pathophysiology of traumatic compartment syndrome and lung contusion.