Key result
IV DDAVP triggers a transient ~74% increase in platelet retention and elevates vWF.
Why the study?
Abnormal plasma levels of von Willebrand factor are accompanied by abnormal platelet function in some disease states, but mechanisms counteracting its pro-adhesive activity are unclear.
Does intravenous DDAVP alter platelet adhesiveness and aggregation in normal male volunteers?
Population
6 normal male volunteers
Comparison
Before and after intravenous administration of 1-deamino 8-D-arginine vasopressin (DDAVP)
Design
Physiological study measuring platelet function variables
Follow-up
60-120 minutes
Authors
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Transient DDAVP effects on platelet retention in volunteers warrant no practice change; leaves open existence of physiological adhesiveness inhibitors.
Does intravenous DDAVP alter platelet adhesiveness and aggregation in normal male volunteers?
The transient increase in platelet retention following DDAVP-induced von Willebrand factor elevation suggests the presence of a physiological inhibitor of platelet adhesiveness.
Porta et al. (1982) studied Healthy volunteers (n=6). 1-deamino 8-D-arginine vasopressin (DDAVP) vs. Baseline (before DDAVP administration) was evaluated on Platelet retention in glass bead columns, platelet aggregation in vitro, beta-thromboglobulin and 6-oxo-prostaglandin F1 alpha. Intravenous administration of DDAVP caused a twofold rise in von Willebrand factor and a transient 74% increase in platelet retention that returned to baseline within 60-120 minutes.
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