title: Exogenous prostacyclin decreases vasoconstriction but not platelet thrombus deposition after arterial injury.
abstract: OBJECTIVE
  The aim of this study was to examine the in vivo effects of increasing doses of prostacyclin (PGI2) on arterial vasoconstriction, platelet deposition and their interrelation after balloon injury of porcine carotid arteries.
  
  
  BACKGROUND
  Extensive platelet deposition and localized vasoconstriction occur acutely after arterial injury in vivo. The platelet deposition and vasoconstriction are directly correlated, and previous studies suggest that platelets may mediate the vasoconstrictive response. However, it is unclear whether vasoconstriction contributes to platelet deposition.
  
  
  METHODS
  Seven pigs received an intravenous infusion of PGI2 at 10 ng/kg per min (PGI2 10), 8 pigs at 50 ng/kg per min (PGI2 50) and 4 pigs at 500 ng/kg per min (PGI2 500); 24 pigs with saline infusion served as a control group.
  
  
  RESULTS
  Vasoconstriction immediately proximal and distal to the balloon-dilated carotid arterial segment where selective endothelial injury occurred was directly related to indium-111-labeled platelet deposition within the dilated segment in both control pigs and PGI2-treated pigs. However, this relation was such that for any given level of platelet deposition relative to control, PGI2 decreased vasoconstriction in a dose-related manner. None of the treatments (PGI2 10, 50 or 500) decreased quantitative 111In-labeled platelet deposition or the proportion of deeply injured arteries with mural thrombus (91%, 70% or 75%, respectively, p = NS) compared with values in control pigs (81%). Thus, vasoconstriction was directly related to platelet deposition in control and PGI2-treated animals, but vasodilation alone did not decrease platelet deposition.
  
  
  CONCLUSIONS
  Intravenous infusion of PGI2 significantly decreases vasoconstriction but not platelet deposition or mural thrombosis after arterial injury by balloon dilation. It is therefore unlikely that vasoconstriction mediates platelet deposition in this model. At hemodynamically tolerated doses, PGI2 infusion probably will not prevent the thrombotic complications associated with angioplasty.
authors.affiliation: Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, Rochester, Minnesota.
authors.forename: J Y
authors.initials: JY
authors.lastname: Lam
authors.forename: J H
authors.initials: JH
authors.lastname: Chesebro
authors.forename: L
authors.initials: L
authors.lastname: Badimon
authors.forename: V
authors.initials: V
authors.lastname: Fuster
mesh_terms: D000818:Animals; D020212:Carotid Artery Injuries; D002341:Carotid Artery Thrombosis / Q000209:etiology / Q000517:prevention & control*; D002404:Catheterization / Q000009:adverse effects; D004305:Dose-Response Relationship, Drug; D011464:Epoprostenol / Q000008:administration & dosage / Q000494:pharmacology*; D007262:Infusions, Intravenous; D010973:Platelet Adhesiveness / Q000187:drug effects*; D013552:Swine; D014661:Vasoconstriction / Q000187:drug effects*
chemical_list: D011464:Epoprostenol