ObjectivesNitric 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.DesignProspective study with consecutive sampling of patients.SettingA university hospital intensive care unit and research laboratories.PatientsSP, 24 patients; IP, 7; and C, 13.InterventionsPlasma measurement of nitrate, lipid peroxides (primary endpoints), andN-hydroxy-l-arginine (secondary end point)Measurements and Main ResultsFor 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.ConclusionsHigh- 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.