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Departments of
*Anesthesiology and Intensive Care Medicine and
Neonatology, University Hospital Charité, Humboldt University, Berlin, Germany
Address correspondence and reprint requests to Michael Schlame, MD, PhD, DEAA, Department of Anesthesiology and Intensive Care Medicine, University Hospital Charité, 10117 Berlin, Germany, Schumannstr. 20/21. Address e-mail to schlamem{at}hss.edu
Cardiopulmonary bypass results in increased plasma activity of phospholipase A2 (PLA2) that appears to be caused by the administration of heparin. High PLA2 activity may be responsible for increased production of eicosanoids and, thus, may be implicated in various pathophysiologic events associated with cardiac surgery. To investigate the site of PLA2 secretion, blood samples were simultaneously collected from the radial artery, the pulmonary artery, and the hepatic vein at 2, 4, 6, and 20 min after systemic heparinization (350 U/kg). Within 2 min of the heparin injection, plasma activity of PLA2 increased 4- to 9-fold and remained so for at least 20 min. Two minutes after the heparin injection, PLA2 was significantly higher in the hepatic vein than in the radial artery (P < 0.01). No such difference was detected between pulmonary and radial arteries. When heparin was added to blood samples in vitro (5100 U/mL), plasma activity of PLA2 did not increase, which suggests that the enzyme was not secreted by blood cells.
Implications: Heparin, given in the dosage required for cardiopulmonary bypass, caused release of phospholipase A2 into the splanchnic circulation.
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