title: Effects of nitric oxide on platelet activation during plateletpheresis and in vivo tracking of biotinylated platelets in humans.
abstract: BACKGROUND
  The use of platelet transfusions has risen considerably over the last few years, which leads to the collection and transfusion of a greater number of donor plateletpheresis units. Plateletpheresis activates platelets in platelet concentrates, which determines the degree of the storage lesion subsequently observed.
  
  
  METHODS
  As nitric oxide (NO) is a potent inhibitor of platelet aggregation and activation, a placebo-controlled crossover trial was performed in healthy young male volunteers to determine whether the NO-donating compound, sodium nitroprusside (SNP), decreases platelet activation during apheresis and whether activated (p-selectin+) platelets circulate in vivo after transfusion. The study also investigated whether nonradioactive biotin labeling of apheresis platelets is feasible for the study of platelet recovery after transfusion in humans.
  
  
  RESULTS
  Platelet activation increased after plateletpheresis in the platelet components, but SNP did not inhibit platelet activation during apheresis, as measured by the percentage of p-selectin expression and the secretion of soluble p-selectin and RANTES. Only a minor increase in p-selectin+ platelets was seen in peripheral blood at 60 minutes after transfusion of the platelets, a rise that was considerably less than that calculated in p-selectin+ platelets if they all were recovered as activated platelets after transfusion. Biotin-labeled platelets averaged 1.5 percent at 10 minutes after transfusion and increased slowly to 2.6 and 3.4 percent after 60 minutes and 24 hours, respectively (p<0.05).
  
  
  CONCLUSIONS
  SNP does not decrease platelet activation during apheresis and subsequent storage, and only a minor proportion of activated (p-selectin+) platelets circulate after transfusion in men. Moreover, biotin labeling of PCs can safely be used in humans for the study of platelet recovery after transfusion, and measuring recovery at 1 hour may lead to an underestimation of the true recovery when activated platelets are transfused.
authors.affiliation: Department of Clinical Pharmacology-TARGET, and Clinical Institute of Medical and Chemical Laboratory Diagnostics, Vienna University Hospital School of Medicine, Austria.
authors.forename: P
authors.initials: P
authors.lastname: Stohlawetz
authors.forename: M
authors.initials: M
authors.lastname: Horvath
authors.forename: T
authors.initials: T
authors.lastname: Pernerstorfer
authors.forename: H
authors.initials: H
authors.lastname: Nguyen
authors.forename: B
authors.initials: B
authors.lastname: Vondrovec
authors.forename: A
authors.initials: A
authors.lastname: Robisch
authors.forename: H G
authors.initials: HG
authors.lastname: Eichler
authors.forename: S
authors.initials: S
authors.lastname: Spitzauer
authors.forename: B
authors.initials: B
authors.lastname: Jilma
mesh_terms: D019921:Biotinylation; D001793:Blood Preservation; D018592:Cross-Over Studies; D004311:Double-Blind Method; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D009569:Nitric Oxide / Q000494:pharmacology*; D009599:Nitroprusside / Q000494:pharmacology; D010865:Pilot Projects; D015539:Platelet Activation / Q000187:drug effects*; D010976:Platelet Count; D017713:Platelet Transfusion; D010983:Plateletpheresis; D012016:Reference Values
chemical_list: D009599:Nitroprusside; D009569:Nitric Oxide