title: Bioactive oxidized lipids in the plasma of cardiac surgical intensive care patients.
abstract: Critical illness is associated with increased oxidative stress that may give rise to the formation of lipid hydroperoxides (LOOH) and various secondary degradation products such as fragmented phosphatidylcholine (FPC) and lipids related to the platelet-activating factor (PAF). Because some oxidized phospholipids are potent proinflammatory agents, we measured the concentration of LOOH, FPC, and PAF-like activity in blood plasma of 36 patients who had undergone cardiac surgery and developed postoperative complications associated with systemic inflammatory response syndrome (SIRS) or multiple organ failure (MOF). These patients were compared to two control groups, namely preoperative patients scheduled for cardiac surgery (n = 13), and postoperative patients without complications (n = 19). Postoperative patents had higher concentrations of LOOH and lower concentrations of FPC than preoperative patients (P < 0.01). However, SIRS and MOF had no significant effect on the concentration of oxidatively modified lipids. This is despite the fact that MOF patients showed evidence of increased lipid peroxidation (7-fold higher ratio of alpha-tocoquinone/alpha-tocopherol compared to control). LOOH correlated positively with the white blood cell count. Postoperative patients had 4-fold higher plasma activities of phospholipase A2 and this activity was further increased in patients with SIRS (P < 0.04). Phospholipase A2 activity correlated negatively with the concentration of FPC. The data suggest that oxidatively modified lipids do not accumulate in patients with SIRS and MOF, perhaps because enhanced peroxidation of lipids is offset by enhanced lipolytic activity.
authors.affiliation: Department of Anesthesiology and Intensive Care Medicine, University Hospital Charite, Humboldt University, Berlin, Germany.
authors.forename: Bettina
authors.initials: B
authors.lastname: Frey
authors.forename: Wolfram
authors.initials: W
authors.lastname: Johnen
authors.forename: Renate
authors.initials: R
authors.lastname: Haupt
authors.forename: Hartmut
authors.initials: H
authors.lastname: Kern
authors.forename: Bernd
authors.initials: B
authors.lastname: Rüstow
authors.forename: Wolfgang J
authors.initials: WJ
authors.lastname: Kox
authors.forename: Michael
authors.initials: M
authors.lastname: Schlame
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D001026:Coronary Artery Bypass; D003422:Critical Care; D005260:Female; D006801:Humans; D050356:Lipid Metabolism; D008054:Lipid Peroxides / Q000097:blood; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D009102:Multiple Organ Failure / Q000097:blood* / Q000503:physiopathology; D010084:Oxidation-Reduction; D010741:Phospholipases A / Q000097:blood; D054467:Phospholipases A2; D011183:Postoperative Complications / Q000097:blood*; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood* / Q000503:physiopathology; D013903:Thoracic Surgery; D013921:Thrombocytopenia / Q000097:blood / Q000503:physiopathology; D014810:Vitamin E / Q000097:blood
chemical_list: D008054:Lipid Peroxides; D008055:Lipids; D014810:Vitamin E; D010741:Phospholipases A; D054467:Phospholipases A2; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase