Reptilase clot retraction test. (Its cofactors and relation to other platelet functions)

C-PRP clotted by reptilase does not retract due to the lack of activation of platelets. In order to support retraction, the platelets must undergo membrane changes resulting in contractile system activation. Only in the presence of aggregating agents capable of eliciting these membrane changes in vitro (e.g. ADP, adrenaline and collagen but not bovine fibrinogen or ristocetin), strong reptilase clot retraction (RCR) occurs. During RCR an aggregating activity, platelet factor 4, and retraction stimulating factor (RSF) were released, but acid phosphatase was not available. Not only inhibitors of platelet adhesion-aggregation reaction (PAAR) but also specific blockers of release are capable of inhibiting RCR. In coagulation disorders RCR was normal in most cases, but in thrombopathies different abnormalities of RCR were found. The RCR defect may be associated not only with a defect in the initial stages of PAAR, but in some instances also with a specific defect in release reaction. Besides inducer--"activated" platelets and their adhesion to polymerizing fibrin, the presence of divalent cations and free thrombocytar--SH groups is necessary for the retraction of reptilase clots.