The Inhaled Nitric Oxide in Acute Respiratory Distress Syndrome: from a Bedside to a Bench.
- Author:
Younsuck KOH
1
Author Information
1. Division of Pulmonary and Critical Care Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
- Publication Type:Multicenter Study ; Original Article
- Keywords:
ARDS;
NO;
Pathogenesis;
Pathophysiology;
Inhalation
- MeSH:
Almitrine;
Anoxia;
Critical Illness;
Humans;
Inflammation;
Inhalation;
Lung;
Lung Injury;
Neutrophils;
Nitric Oxide*;
Oxygen;
Peroxidase;
Phenylephrine;
Positive-Pressure Respiration;
Pulmonary Artery;
Respiratory Distress Syndrome, Adult*;
Vasodilation
- From:The Korean Journal of Critical Care Medicine
2001;16(2):65-74
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Because inhaled nitric oxide (NO) induces selective vasodilation of well-ventilated lung regions diverting pulmonary artery blood flow towards these well-ventilated alveoli, it has been applied to some of ARDS patients, who show severe hypoxemia despite of positive pressure ventilation with moderate to high positive end-expiratory pressure. The beneficial effect of inhaled NO on oxygenation was lower than 5 ppm of inhaled NO and the maximum effect was about 10 ppm in patients with ARDS according to the studies. Combinations of inhaled NO with various therapies, such as the use of intravenous almitrine or phenylephrine, and prone positioning may produce additive effects on oxygenation. Approximately 65% of patients had response to inhaled NO in studies of critically ill patients with ARDS who were ventilated with less than 40 ppm of inhaled NO. However, there was no survival benefit by inhaled NO in a multicenter phase 2 trial with 177 patients of non-septic ARDS. It is unclear whether inhaled NO exerts detrimental or beneficial effects in the pathogenesis of ARDS. Laboratory studies suggest that inhaled NO has important effects in reducing some forms of lung and tissue injury. If these effects are clinically significant, early and continued therapy with inhaled NO could potentially reduce the severity of some forms of lung injury. In contrast, NO and nitrite interacted with neutrophil myeloperoxidase to stimulate oxidative reactions during inflammation. In summary, NO inhalation would be acceptable as a rescue therapy in severe ARDS without serious complications related to the application. In addition, the effect of inhaled NO on the pathophysiology of ARDS should be elucidated.
