title: High and low response in relation to nitric oxide formation but not to lipid peroxidation in patients with sepsis.
abstract: OBJECTIVE
  Nitric oxide overproduction in sepsis syndrome was suspected to be responsible for hemodynamic derangement and, by induction of lipid peroxidation, for tissue damage. Therefore, nitric oxide formation and lipid peroxidation were quantified in septic patients (SP) vs. patients with localized infection (IF) or without inflammation (C). Nitric oxide formation in sepsis was additionally compared with data for clinical status.
  
  
  METHODS
  Prospective study with consecutive sampling of patients.
  
  
  METHODS
  A university hospital intensive care unit and research laboratories.
  
  
  METHODS
  SP, 24 patients; IP, 7; and C, 13.
  
  
  METHODS
  Plasma measurement of nitrate, lipid peroxides (primary endpoints), and N-hydroxy-L-arginine (secondary end point)
  
  
  RESULTS
  For nitrate, there was a sequence of C < IP = SP. Among SP, one group with significantly higher nitrate (high-responders for nitric oxide; SP-HR) vs. IP and C and a second group (low-responders; SP-LR) with increased concentration only vs. C could be identified. For SP-HR vs. IP, a strong time kinetics in nitric oxide formation was obvious, indicated by significant nitrate increase already 1 day before sepsis started, tripling up to the peak concentration, and then a lowering but still increased value on the first day after sepsis. N-hydroxy-L-arginine was significantly increased in SP-HR vs. C. For lipid peroxides, the concentrations were comparable in SP and IP, but both significantly increased vs. C. Clustering and coincident kinetics of lipid peroxidation related to nitric oxide were not obvious. Furthermore, there was no strong correlation of clinical data and nitric oxide clustering in sepsis.
  
  
  CONCLUSIONS
  High- and low-responders for nitric oxide were identified among septic patients. This finding was not associated with significant differences in lipid peroxidation or clinical data.
authors.affiliation: Medizinische Klinik, Universitätsklinikum Charité, Humboldt Universität zu Berlin, Germany. ingolf.schimke@charite.de
authors.forename: Ingolf
authors.initials: I
authors.lastname: Schimke
authors.forename: Nadja
authors.initials: N
authors.lastname: Richter
authors.forename: Helmar
authors.initials: H
authors.lastname: Wauer
authors.forename: Ute
authors.initials: U
authors.lastname: Rohr
authors.forename: Ann-Sofi
authors.initials: AS
authors.lastname: Petersson
authors.forename: Ake
authors.initials: A
authors.lastname: Wennmalm
authors.forename: Hermann
authors.initials: H
authors.lastname: Kuppe
authors.forename: Wolfgang J
authors.initials: WJ
authors.lastname: Kox
mesh_terms: D000328:Adult; D000368:Aged; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood; D016022:Case-Control Studies; D005260:Female; D008401:Gas Chromatography-Mass Spectrometry; D006801:Humans; D015227:Lipid Peroxidation; D008054:Lipid Peroxides / Q000097:blood; D008297:Male; D008875:Middle Aged; D009566:Nitrates / Q000097:blood; D009569:Nitric Oxide / Q000097:blood*; D011446:Prospective Studies; D018709:Statistics, Nonparametric; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood* / Q000382:microbiology
chemical_list: D008054:Lipid Peroxides; D009566:Nitrates; D009569:Nitric Oxide; D001120:Arginine