Abstract

Platelets play a pivotal role when blood or blood vessels are injured. If inflammation is viewed broadly as the response of tissue to injury, the hemostatic function of platelets can be considered a component of an inflammatory process. Platelets in flowing blood can adhere to the strands of connective tissue. Adhesion is also observed in vitro. It can occur in EDTA platelet-rich plasma, showing that divalent cations are not required. The material to which platelets adhere is not destroyed by prolonged digestion with collagenase and is digested by trypsin. Aggregation in platelet suspensions can be followed by the continuous recording of light transmission or optical density, usually at 37°C. ADP is a potent platelet aggregating agent. Aggregation can be induced by stirring fine particles of connective tissue with citrated or heparinized platelet-rich plasma, after a lag period that varies with the concentration of particles up to several minutes. Aggregation seems to be caused entirely by the release of platelet ADP. When low concentrations of thrombin are stirred with citrated platelet-rich plasma, the resulting aggregation is often reversible. With higher concentrations, a double wave may be seen. Still higher concentrations induce coagulation. The second wave may be associated with the release of catecholamines from platelets.

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