title: Intravenous prostaglandin E1 reduces soluble vascular cell adhesion molecule-1 in peripheral arterial obstructive disease.
abstract: OBJECTIVE
  Elevated levels of soluble (s) vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1, pointing to activation of cells involved in vascular inflammation, have been previously reported in peripheral arterial obstructive disease (PAOD). We tested the hypothesis that intravenous prostaglandin E(1) (PGE(1)) treatment, which produces clinical benefits in this condition, might decrease such levels.
  
  
  METHODS
  Ten subjects (age range 58 +/- 10 years, 6 male, 4 female) with characterized Fontaine stage IIa to IV PAOD (ankle/arm pressure index <0.96) were entered into a treatment protocol with twice daily intravenous infusions of PGE(1) (alprostadil) at 120 microg per day, repeated for 10 consecutive days. Preinfusion and postinfusion plasma samples were stored for blind enzyme immunoassays of soluble adhesion molecules and the fibrinolytic marker tissue plasminogen activator, type-1 plasminogen-activator inhibitor, and D -dimer.
  
  
  RESULTS
  Estimates of severity of pain at rest, consumption of analgesics, magnitude of trophic lesions, remission to lower Fontaine stages, and favorable changes in the venoarteriolar reflex documented significant beneficial effects of the treatment. Significant (P <.01) pretreatment and posttreatment reductions of in all soluble markers explored were found. Particularly, sVCAM-1 exhibited a significant decrease after each infusion, which was sustained at the last day of treatment (from 854 +/- 214 ng/mL to 775 +/- 215 ng/mL across the first infusion, from 773 +/- 146 ng/mL to 680 +/- 110 ng/mL across the last infusion).
  
  
  CONCLUSIONS
  Thus a global decrease of vascular cell activation appears to occur as a result of PGE(1) administration and may contribute to the observed clinical benefits in PAOD.
authors.affiliation: Laboratory for Thrombosis and Vascular Research, CNR Institute of Clinical Physiology, Pisa, Italy.
authors.forename: J
authors.initials: J
authors.lastname: Gianetti
authors.forename: M
authors.initials: M
authors.lastname: De Caterina
authors.forename: T
authors.initials: T
authors.lastname: De Cristofaro
authors.forename: B
authors.initials: B
authors.lastname: Ungaro
authors.forename: R D
authors.initials: RD
authors.lastname: Guercio
authors.forename: R
authors.initials: R
authors.lastname: De Caterina
mesh_terms: D000368:Aged; D000527:Alprostadil / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D001157:Arterial Occlusive Diseases / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy*; D005080:Exercise Test / Q000706:statistics & numerical data; D005260:Female; D005342:Fibrinolysis / Q000187:drug effects; D006801:Humans; D007262:Infusions, Intravenous; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D010147:Pain Measurement; D016491:Peripheral Vascular Diseases / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy*; D016896:Treatment Outcome; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood* / Q000187:drug effects
chemical_list: D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D000527:Alprostadil