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Platelet Interactions with the Endothelium and the Subendothelium: the Role of Thrombin and Prostacyclin

 

作者: Jean-Pierre Cazenave,   Elisabetta Dejana,   Raelene Kinlough-Rathbone,   Marian A. Packham,   Fraser Mustard,  

 

期刊: Pathophysiology of Haemostasis and Thrombosis  (Karger Available online 1979)
卷期: Volume 8, issue 3-5  

页码: 183-192

 

ISSN:1424-8832

 

年代: 1979

 

DOI:10.1159/000214310

 

出版商: S. Karger AG

 

关键词: Platelet;Endothelium;Subendothelium;Adhesion;Release reaction;Thrombin;Prostacyclin;Cyclic AMP

 

数据来源: Karger

 

摘要:

The adherence of 51Cr-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 (PGE1, PGI2 or dipyridamole). These agents, however, did not abolish platelet adherence to the subendothelium. Aspirin treatment of the vessel wall was used to block PGI2 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 PGI2 formation by the vessel wall is the mechanism that prevents platelet adherence to normal endothelium. In addition, PGI2 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

 

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