Contribution of the subendothelium to prostacyclin release after vascular injury.
PGI2 release from intact and de-endothelialized vascular segments has been evaluated in a template device to determine the early response of the vessel wall to physical injury. The luminal surfaces of mechanically denuded areas of vascular segments released high concentrations (450 nM) of 6-keto-PGF1 alpha, the stable hydrolysis product of PGI2, in the initial hours after injury. Later the denuded regions of vessels had blunted 6-keto-PGF1 alpha release under basal and stimulated conditions equal to 5% to 25% of that obtained from adjacent intact regions. The recovery of 6-keto-PGF1 alpha from de-endothelialized segments suggests that subendothelial components of the vessel wall contribute to the PGI2 released at the luminal surface. These observations on intact and damaged vessels may have important implications with respect to vascular function after injury and the resultant platelet-vessel wall interactions.
D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism*; D000818:Animals; D001011:Aorta / Q000293:injuries* / Q000378:metabolism / Q000648:ultrastructure; D000001:Calcimycin / Q000494:pharmacology; D002417:Cattle; D004727:Endothelium / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D011464:Epoprostenol / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D008855:Microscopy, Electron, Scanning; D011453:Prostaglandins / Q000378:metabolism*; D011651:Pulmonary Artery / Q000293:injuries* / Q000378:metabolism
D011453:Prostaglandins; D000001:Calcimycin; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol