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DDAVP's shortening of the bleeding time seems due to plasma von Willebrand factor
K H Beck1, U Bleckmann, P Mohr
1Department of Transfusion Medicine and Hemostaseology, Klinikum, Philips, University Marburg, Germany.
The pathomechanism of desmopressin (DDAVP) dependent shortening of the acetylsalicylic acid (ASA) prolonged bleeding time (BT) is still unclear. The mechanism of action is supposed to be related to the plasma levels of von Willebrand factor (vWf), but a platelet effect is also discussed. We tried to investigate whether this effect of DDAVP might be due to either plasma vWF or platelets or both. We measured the effect of DDAVP (0.4 micrograms/ml bw in 250 ml 0.9% NaCl) on the Thrombostat 4000 (in vitro bleeding test (IVBT)) after each of 16 volunteers ingested 100 mg of ASA twice. To measure the possible effect of DDAVP on plasma and platelets separately, a mixture of 800 microliters of platelet poor plasma (PPP) or 200 microliters of isolated platelets after DDAVP, respectively, was prepared and the IVBT monitored. Two hundred microliters of PPP or platelets, respectively, served as a control. In an additional experiment, vWF concentrate (12 U/ml) dissolved in 200 microliters of PPP after ASA ingestion, as described above, was added to 800 microliters of citrated whole blood from the same volunteers. The addition of PPP after DDAVP as well as the PPP or PRP after ASA enriched with vWf led to a significant shortening of the IVBT in comparison to the control, indicating that the effect of DDAVP on the prolonged BT seems to be an isolated effect of plasma vWf. By adding platelets we were not able to show a direct effect of DDAVP on platelets.
The pathomechanism of desmopressin (DDAVP) dependent shortening of the acetylsalicylic acid (ASA) prolonged bleeding time (BT) is still unclear. The mechanism of action is supposed to be related to the plasma levels of von Willebrand factor (vWf), but a platelet effect is also discussed. We tried to investigate whether this effect of DDAVP might be due to either plasma vWF or platelets or both. We measured the effect of DDAVP (0.4 micrograms/ml bw in 250 ml 0.9% NaCl) on the Thrombostat 4000 (in vitro bleeding test (IVBT)) after each of 16 volunteers ingested 100 mg of ASA twice. To measure the possible effect of DDAVP on plasma and platelets separately, a mixture of 800 microliters of platelet poor plasma (PPP) or 200 microliters of isolated platelets after DDAVP, respectively, was prepared and the IVBT monitored. Two hundred microliters of PPP or platelets, respectively, served as a control. In an additional experiment, vWF concentrate (12 U/ml) dissolved in 200 microliters of PPP after ASA ingestion, as described above, was added to 800 microliters of citrated whole blood from the same volunteers. The addition of PPP after DDAVP as well as the PPP or PRP after ASA enriched with vWf led to a significant shortening of the IVBT in comparison to the control, indicating that the effect of DDAVP on the prolonged BT seems to be an isolated effect of plasma vWf. By adding platelets we were not able to show a direct effect of DDAVP on platelets.