THE LUPUS ANTICOAGULANT DOES NOT INHIBIT THE RELEASE OF PROSTACYCLIN FROM HUMAN ENDOTHELIAL CELLS
Decreased endothelial cell production of prostacyclin (PGI2) in response to the lupus anticoagulant has been previously demonstrated, and postulated to have a causal relationship to the thrombotic events associated with the lupus anticoagulant. Five patients who exhibited the anticoagulant were studied in an effort to determine if a relationship exists between exposure of endothelial cells to the lupus anticoagulant and decreased production of prostacyclin (PGI2). Human endothelial cells derived from human umbilical vein grown in culture were exposed to IgG fractions of patient plasmas containing the lupus anticoagulant. The amount of PGI2 released was determined by radioimmunoassay for 6-keto-PGF-l-alpha. The average PGI2 release in the controls was 20.6 picomol/500,000 endothelial cells, whereas those cells exposed to the lupus anticoagulant had a range of 25 to 114 picmol/500,000 cells. We were unable to demonstrate inhibition of the release of PGI2 by human endothelial cells, following exposure to the lupus anticoagulant.(Supported by NIH Grant HL 33723-2 and a Specialized Center of Research in Thrombosis Award HL 35058-01 from the National Heart, Lung and Blood Institute.)