Hemostasis

Platelets maintain capillary intergrity. In The absence of platelets, red cells will migrate through the vessel walls in large numbers. In addition, platelets play a major role in the hemostatic process.

Within one to two seconds after injury to a blood vessels, platelets come in contact with, and adhere to the injured tissues (platelets adhesiveness). Serotonin (which may assist in vasoconstriction), and adenosine diphosphate (ADP), are released by the platelets. the ADP released by the platelets, and also by the injured tissues, causes the platelets to stick to one another (in vivo, this termed platelet cohesiveness; in vitro, this characteristic is known as platelet aggregation), forming a platelet plug.

Thrombin is generated, due to the presence of tissue thromboplastin (F.III) from the damage cells, and activation of the intrinsic system by collagen. The thrombin causes a denser, irreversible cohesion of the platelets. The platelets undergo disruption, releasing more ADP and a phospholipid termed platelet factor 3. This phospholipid is then free to act in the intrinsic coagulation system. The thrombin present is free to convert fibrinogen to fabrin, and this network stabilizes the already formed platelet plug. The protien, thrombasthenin, present in the platelets, further strengthens this hemostatic plug. In Vitro, this last step is termed clot retraction, and may be observed when blood is allowed to clot in tube. After a period of time, the clot will decrease in size and clear serum will be expressed from the clot.

Author: Dayyal Anand