The effect of aspirin inhibition of PGI2 production on platelet adherence to normal and damaged rabbit aortae

These experiments were designed to investigate whether or not PGI2 production by vessel walls is responsible for their non-thrombogenic property. Adherence of rabbit platelets to the endothelium and sub-endothelium of the rabbit aorta was studied in vitro and in vivo when PGI2 production by the vessel wall was inhibited by aspirin. For in vitro studies, everted segments of rabbit aorta were mounted on a probe and rotated in a suspension of washed 51Cr-labeled platelets; the number of adherent platelets was calculated from the radioactivity associated with the platelets adherent to the segments. (This method measures the adherence of individual platelets, not platelet thrombi.) When adherence to the subendothelium was to be measured, the endothelium was removed by passage of a balloon catheter. The platelets and/or the vessel wall were pretreated with aspirin (1 mM and 2 mM respectively), washed and resuspended in fresh medium before adherence was measured. For in vivo studies, 51Cr-labeled platelets were injected into rabbits and the aortae were perfused and fixed in situ 20 min after administration of 25 or 100 mg of aspirin per kg. Platelet accumulation on both undamaged and de-endothelialized aortae was examined. PGI2-like activity produced by the vessel walls was measured by a bioassay; it was demonstrated that the aspirin treatment abolished the ability of the vessels to form PGI2, even when sodium arachidonate was supplied as a precursor. Both in vitro and in vivo prevention of PGI2 production did not affect the number of platelets that adhered to the endothelium or the subendothelium under these experimental conditions. Thus it is unlikely that the production of PGI2 by the vessel wall prevents platelets from adhering to the endothelium or subendothelium, although PGI2 may limit subsequent thrombus formation at an injury site.