Abstract
A large number of studies show elevated levels of nitric oxide (NO) in infective syndromes, but there is an insufficient number of studies which have investigated serum levels of NO in patients with acute respiratory distress syndrome (ARDS), especially in relation to survival. Hence, we created a study with the aim of determining the NO levels in relation to ARDS survival.Serum levels of NO were measured by Griess reaction in 29 patients [16 men (55%), mean age years 52.72±18]. All data were statistically analyzed using one way ANOVA.Our results show significantly higher serum NO levels in ARDS survivors compared to ARDS non-survivors, (p < 0.05). We conclude that higher serum levels of NO are strongly associated with better clinical outcomes, including increased survival.
Highlights
(15) Inhibition of these proteins may contribute to the proinflammatory environment believed to be pathogenic in Acute respiratory distress syndrome (ARDS). [16,17,18] Peroxynitrite cannot be measured directly because of its short half-life, but its presence can be inferred by measuring metabolites such as NO2– and NO3–. [15] There is a small number of studies which investigated serum levels of nitric oxide (NO) in patients with ARDS caused by H1N1 pneumonia and in relation to survival
Extended analysis of NO serum levels in patients with ARDS caused by H1N1 pneumonia showed the following results: H1N1-ARDS survivor patients had significantly higher serum NO levels compared to H1N1-ARDS non-survivor patients
(1) The main finding of this study is that H1N1-ARDS survivors have significantly higher serum levels of NO
Summary
Acute respiratory distress syndrome (ARDS) is an acute, diffuse, inflammatory lung injury that leads to increased pulmonary vascular permeability, increased lung weight, and a loss of aerated tissue. [1] Clinical hallmarks of ARDS are hypoxemia and bilateral radiographic opacities, while the pathological hallmark is diffuse alveolar damage (i.e., alveolar edema with or without focal hemorrhage, acute inflammation of the alveolar walls, and hyaline membranes); without mechanical ventilation most patients would die. [2] It is well known that mediators of inflammation have a significant role in ARDS. [3,4,5] Many of them, such as interferon-γ, interleukin-1β (IL-1β), and tumor necrosis factor-α, lead to increased production of nitric oxide (NO) which causes oxidative injury. [6,7] Nitric oxide is a reactive molecule produced by nitric oxide synthase (NOS) enzymes in a variety of cells. [8] Three distinct forms of NOS have been identified; endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS). [9] Both eNOS and nNOS are constitutive forms of NOS (cNOS) that produce small amounts of NO for short periods of time when appropriately stimulated. Acute respiratory distress syndrome (ARDS) is an acute, diffuse, inflammatory lung injury that leads to increased pulmonary vascular permeability, increased lung weight, and a loss of aerated tissue. [9] Both eNOS and nNOS are constitutive forms of NOS (cNOS) that produce small amounts of NO for short periods of time when appropriately stimulated. [6] Oxidant-mediated tissue injury is likely to be important in the pathogenesis of ARDS. [12] Nitric oxide readily reacts with superoxide ion to form a highly reactive intermediate known as peroxynitrite. [15] There is a small number of studies which investigated serum levels of NO in patients with ARDS caused by H1N1 pneumonia and in relation to survival. The first hypothesis was that NO serum levels would be higher in ARDS patients compared to the healthy population. The second hypothesis was that NO serum levels would be higher in ARDS survivors than in nonsurvivors
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