DEMONSTRATION THAT VENOUS OCCLUSION FAILS TO RELEASE VON-WILLEBRAND-FACTOR MULTIMERS

The acute simultaneous release of tissue plasminogen activator (t-PA) and von Willebrand factor (vWF) from endothelial cells in response to a variety of agonists including thrombin, DDAVP, histamine and adrenal in has been described In the present study we investigated the effect of venous occlusion on the circulating levels of t-PA and vWF, as well as the molecular organization of vWF in 20 normal subjects. After occ lusion a significant increase in plasma t-PA levels was observed even after the values were corrected for haemoconcentration. Venous occlusi on also enhanced plasma vWF values, but the increase was abolished whe n the correction for haemoconcentration was introduced. Following veno us occlusion, no circulating abnormally large vWF multimers were detec ted in the subjects studied These forms are normally not present in th e circulation and are released from endothelial cells through the regu lated vWF pathway; their absence therefore seems to demonstrate that t his pathway is not activated after venous occlusion Since occlusion do es not enhance VWF synthesis, the increase in vWF observed in the subj ects investigated may be fully attributed to haemoconcentration.