Platelet Interactions with the Endothelium and the Subendothelium: the Role of Thrombin and Prostacyclin Journal Articles uri icon

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  • The adherence of <sup>51</sup>Cr-labeled platelets to rabbit aortae everted on probes rotated in platelet-red cell suspensions has been measured. Platelet adherence to the subendothelium exposed by passage of a balloon catheter before everting the aortae was inhibited by compounds that increase platelet cyclic AMP levels (PGE<sub>1</sub>, PGI<sub>2</sub> or dipyridamole). These agents, however, did not abolish platelet adherence to the subendothelium. Aspirin treatment of the vessel wall was used to block PGI<sub>2</sub> production; platelet adherence to the surface of the ‘undamaged’ aorta and the subendothelium was studied following this treatment. Since aspirin treatment of the ‘undamaged’ vessel wall did not cause platelets to adhere to it, it seems unlikely that PGI<sub>2</sub> formation by the vessel wall is the mechanism that prevents platelet adherence to normal endothelium. In addition, PGI<sub>2</sub> formation by the vessel wall does not appear to influence platelet adherence to the subendothelium, since adherence was not increased by aspirin treatment of the damaged wall. Thrombin treatment of the ‘undamaged’ vessel wall increased platelet adherence to the surface, but the adherent platelets were seen to be adherent only to small areas where the endothelium was lost or damaged. Heparin reversed the effect of thrombin. Similar results were found when the subendothelium was exposed to thrombin or thrombin and heparin.


  • Rathbone, Raelene Lorna
  • Cazenave, Jean-Pierre
  • Dejana, Elisabetta
  • Kinlough-Rathbone, Raelene
  • Packham, Marian A
  • Mustard, Fraser

publication date

  • 1979