Summary
Dipyridamole (Persantin) is reported to prolong platelet survival and inhibit embolism
in patients with prosthetic heart valves, but its mechanism of action is unknown.
Fifty jxM dipyridamole failed to reduce the high percentage of platelets retained
when heparinized human blood was passed through a glass bead column, but prolonged
the inhibition of retention caused by disturbing blood in vitro. Possibly the prostheses
act like disturbance. Although RA 233 was as effective as dipyridamole in inhibiting
the return of retention, it was less effective in preventing the uptake of adenosine
into erythrocytes, and more active in inhibiting ADP-induced aggregation and release.
Thus there is no simple relation between these drug effects.