OBJECTIVE: To investigate the relationship between nitric oxide production, endotoxemia, and hemodynamic alterations in human septic shock. DESIGN: Prospective study. SETTING: A 32-bed intensive care unit in a university referral hospital. PATIENTS: Two groups of septic patients with shock (n = 13) or without shock (n = 16) and an additional group of nonseptic patients as control group (n = 25). MEASUREMENTS: Plasma nitrite and nitrate concentrations were measured as an index of nitric oxide generation. Nitrite and nitrate concentrations were correlated with plasma endotoxin and hemodynamic variables. MAIN RESULTS: Increased plasma nitrite and nitrate concentrations were found in patients with septic shock (p < .01). Nitrite and nitrate correlated directly with endotoxin concentration (r2 = .21, p < .05) and cardiac output (r2 = .49, p < .05), and inversely with systolic blood pressure (r2 = .24, p < .01). CONCLUSIONS: This study demonstrated the activation of the L-arginine:nitric oxide pathway in human endotoxemic septic shock, suggesting that nitric oxide may be an important mediator of the hemodynamic disturbances in this pathophysiologic situation.
OBJECTIVE: To investigate the relationship between nitric oxide production, endotoxemia, and hemodynamic alterations in humanseptic shock. DESIGN: Prospective study. SETTING: A 32-bed intensive care unit in a university referral hospital. PATIENTS: Two groups of septic patients with shock (n = 13) or without shock (n = 16) and an additional group of nonseptic patients as control group (n = 25). MEASUREMENTS: Plasma nitrite and nitrate concentrations were measured as an index of nitric oxide generation. Nitrite and nitrate concentrations were correlated with plasma endotoxin and hemodynamic variables. MAIN RESULTS: Increased plasma nitrite and nitrate concentrations were found in patients with septic shock (p < .01). Nitrite and nitrate correlated directly with endotoxin concentration (r2 = .21, p < .05) and cardiac output (r2 = .49, p < .05), and inversely with systolic blood pressure (r2 = .24, p < .01). CONCLUSIONS: This study demonstrated the activation of the L-arginine:nitric oxide pathway in humanendotoxemic septic shock, suggesting that nitric oxide may be an important mediator of the hemodynamic disturbances in this pathophysiologic situation.
Authors: Moshe Hersch; Jeremy A Scott; Gabriel Izbicki; David McCormack; Gedeminas Cepinkas; Marlies Ostermann; William J Sibbald Journal: Intensive Care Med Date: 2005-06-15 Impact factor: 17.440
Authors: Tjasa Hranjec; Brian R Swenson; Lesly A Dossett; Rosemarie Metzger; Tanya R Flohr; Kimberley A Popovsky; Hugo J Bonatti; Addison K May; Robert G Sawyer Journal: J Am Coll Surg Date: 2010-05 Impact factor: 6.113
Authors: J A Avontuur; T C Stam; M Jongen-Lavrencic; J G van Amsterdam; A M Eggermont; H A Bruining Journal: Intensive Care Med Date: 1998-07 Impact factor: 17.440
Authors: Mary Anne M Morgan; Lauren M Frasier; Judith C Stewart; Cynthia M Mack; Michael S Gough; Brian T Graves; Michael J Apostolakos; Kathleen P Doolin; Denise C Darling; Mark W Frampton; Anthony P Pietropaoli Journal: Crit Care Med Date: 2010-04 Impact factor: 7.598