Summary
We have studied the accumulation of washed platelets on collagen-coated glass from
flowing platelet-red blood cell suspensions in the presence and absence of drugs.
Glass tubes were 10 cm long and the flow rate was 1 ml/min, 80 s-1. For all experiments, platelet accumulation was greatest near the tube’s inlet with
a continuous decrease to the exit. A common feature, of those drug treatments which
lead to reduced accumulation at the inlet, was an increase in outlet accumulation
when compared with outlet control values. Platelet-collagen adhesion resulted in maximal
release of 3H-serotonin in the presence of agents that prevent platelet aggregation on collagen.
Only drug treatment known to raise cAMP levels (PGE1 and dipyridamole) or prevent the formation of prostaglandins and thromboxanes (sulfinpyrazone,
indomethacin and ASA) were found to inhibit aggregate growth. Platelet aggregation
on collagen in the absence of thrombin likely proceeds through the liberation of prostaglandins
and thromboxanes from surface-bound platelets into the flow where they may stimulate
flow-bom cells. An alternate hypothesis is that such treatments affect the release
of a-granule components necessary for aggregation.
Keywords
Platelet adhesion - Platelet aggregation - Platelet release - Collagen - Anti-thrombotic
drugs
