Effect of prostacyclin on platelets, polymorphonuclear cells, and heterotypic
cell aggregation during hemofiltration.
Author(s): Kozek-Langenecker SA(1), Spiss CK, Michalek-Sauberer A, Felfernig M, Zimpfer M.
Affiliation(s): Author information:
(1)Department of Anesthesiology and Intensive Care, University of Vienna School
of Medicine, Austria. sibylle.kozek@univie.ac.at
Publication date & source: 2003, Crit Care Med. , 31(3):864-8
OBJECTIVES: Hemodialysis activates both platelets and leukocytes, which play a
role in the development of multiple organ dysfunctions in critically ill
patients. Prostacyclin inhibits both cell types. To examine the hypothesis that
prostacyclin prevents cellular activation during clinical hemofiltration, we
investigated the expression of activation markers on platelets and leukocytes
using whole blood flow cytometry.
DESIGN: Prospective, randomized, double-blind, controlled trial.
SETTING: Intensive care unit.
PATIENTS: A total of 24 consecutive, critically ill, mechanically ventilated
patients with acute renal failure secondary to sepsis or major surgery.
INTERVENTIONS: For anticoagulation during hemofiltration, patients received
either unfractionated heparin or unfractionated heparin and prostacyclin (5 ng x
kg(-1) x min(-1)). Anticoagulants were administered into the extracorporeal
circuit before the hemofilter. Blood samples were obtained from an arterial
catheter before hemofiltration and from the inlet and outlet lines of the
extracorporeal circuit at 1 and 24 hrs during hemofiltration.
MEASUREMENTS AND MAIN RESULTS: Expression of GP IIb-IIIa and P-selectin on
adenosine diphosphate-activated platelets and platelet-leukocyte aggregation were
significantly lower after the passage of blood through the hemofilter in patients
receiving an extracorporeal infusion of prostacyclin plus heparin when compared
with control patients receiving heparin only. There were no statistically
significant differences in the expression of CD11b on leukocytes between the two
groups.
CONCLUSIONS: These findings suggest that prostacyclin reversibly inhibits
platelet function by diminishing the expression of platelet fibrinogen receptors
and P-selectin and reduces heterotypic platelet-leukocyte aggregation during
clinical hemofiltration. However, prostacyclin fails to inhibit leukocyte
activation at clinically relevant doses.
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