Abstract
The behavior of stretched out human platelets in different stages of blood clotting has been observed with the electron microscope. In the early stages of coagulation the morphologically intact platelets apparently act as centers of orientation and condensation of the fibrin fibrils. This effect is not found in platelets which have previously undergone extensive damage or disintegration. In more advanced stages of clotting, many platelets remain normal, showing their attachment to the fibrin, while others have disintegrated and appear as residual dense bodies. The probable action of platelets in the retraction and syneresis of the blood clot is discussed. It is suggested that at the surface of the morphologically intact platelets, adhesion forces develop which hold and orient the molecular chains of fibrin increasing the number of interacting junctions and producing syneresis. On the contrary, the platelets which have suffered an injury which alters these surface adhesive properties do not interact with the fibrin fibrils and, as a result, the mechanism of clot retraction is impaired.

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