Summary
The release of prostacyclin (PGI2) and von Willebrand factor (vWF) from human umbilical vein endothelial cells (HUVEC)
was examined to determine if aprotinin had any effects on these endothelial cell reactions.
These end-points were chosen to indicate if this serine protease inhibitor caused
alterations in the control of haemostatic function by endothelium, in the light of
the improvement in haemostasis seen in patients given aprotinin therapy at the time
of open heart surgery. Stimuli used to promote secretion of prostacyclin and vWF were
human α-thrombin, histamine, protamine sulphate, poly-L-lysine and phor-bol myristate
acetate. Aprotinin (30 pM) had no significant effect on the basal or stimulated release
of PGI2 or vWF from HUVEC.
