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Platelet activation and fibrin formation occur in thrombo-embolism, arterial disease, and intravascular coagulation. Selective involvement in certain disease entities and combined involvement in others has been suggested on the basis of turnover studies. The development in this laboratory of sensitive and specific radioimmunoassays for two released platelet proteins, PF4 and βTG, and the availability of the radioimmunoassay for FPA as an index of fibrin formation have allowed studies of the physiologic basis for differential involvement of platelets and fibrin formation. Simultaneous measurement of platelet activation, monitored by radioimmunoassay for PF4 and βTG as well as aggregometry and 14C-serotonin (5HT) release, and FPA cleavage were carried out in citrated platelet rich plasma, whole blood and gel-filtered platelets. Collagen and ADP aggregated platelets and released 5HT, PF4 and βTG without detectable FPA cleavage indicating that thrombin action on fibrinogen is not involved in aggregation or release induced by these agents. Thrombin cleaved FPA at concentrations 100-fold less than those required for platelet protein release, and platelet protein release could be detected at lower thrombin concentrations than 5HT release. This might be due to greater sensitivity of the PF4 and βTG assays in detecting release or to different mechanisms of release of the proteins and 5HT. These results suggest that, in clinical samples, elevated FPA with normal PF4 and βTG might be due to concentrations of circulating thrombin sufficient to cleave FPA but too low to induce platelet release, and that the converse situation, with elevated PF4 and βTG but normal FPA might imply platelet activation by exposed subendothelial collagen with no thrombin action.

Simultaneous Measurement of Platelet Factor 4 (PF4) and β-Thromboglobulin (βTG) Release and Fibrinopeptide A (FPA) Cleavage