Inhalation of nitric oxide in acute lung injury: results of a European multicentre study

Lundin, S.; Mang, H.J.; Smithies, Mark; Stenqvist, O.; Frostell, Claes

doi:10.1007/s001340050982

Cited by 371 publications

(182 citation statements)

References 18 publications

Supporting

Mentioning

160

Contrasting

Unclassified

Order By: Relevance

“…In randomized clinical trials, inhaled nitric oxide was associated with a transient improvement in oxygenation in adults with ARDS without any survival benefit. [16][17][18][19][20] In a systematic review and meta-analysis of patients with acute lung injury or ARDS from 12 trials, inhaled nitric oxide was associated with modest improvements in oxygenation (13% increase in P aO 2 /F IO 2 until days 3-4 of administration), no effect on mean pulmonary artery pressure, and no effect on survival or duration of mechanical ventilation. 21 Period 1 is defined as prior to the start of the epoprostenol infusion, and period 2 is defined as during the epoprostenol infusion.…”

Section: Discussionmentioning

confidence: 99%

Predictors of Outcome in 216 Subjects With ARDS Treated With Inhaled Epoprostenol

Pacheco

Arnold²,

Skrupky³

et al. 2013

Respir Care

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Predictors of Outcome in 216 Subjects With ARDS Treated With Inhaled Epoprostenol

Pacheco

Arnold²,

Skrupky³

et al. 2013

Respir Care

View full text Add to dashboard Cite

“…Inhaled NO therapy did not affect the duration of ventilatory support or mortality in 2 single-center pilot trials 61,62 and in 3 multicenter randomized trials. [63][64][65] Because most patients dying from acute respiratory distress syndrome suffer from multiple organ failure, it is unlikely that the beneficial effects of a lung-selective therapy such as inhaled NO will alter the overall survival rate.…”

Section: Inhaled No and Acute Respiratory Distress Syndromementioning

confidence: 99%

Inhaled Nitric Oxide

2004

View full text Add to dashboard Cite

Since the recognition of nitric oxide (NO) as a key endothelial-derived vasodilator molecule in 1987, the field of NO research has expanded to encompass many areas of biomedical research. It is now well established that NO is an important signaling molecule throughout the body. The therapeutic potential of inhaled NO as a selective pulmonary vasodilator was suggested in a lamb model of pulmonary hypertension and in patients with pulmonary hypertension in 1991. 1,2 Because NO is scavenged by hemoglobin (Hb) on diffusing into the blood and is thereby rapidly inactivated, the vasodilatory effect of inhaled NO is limited largely to the lung. This is in contrast to intravenously infused vasodilators that can cause systemic vasodilation and severe systemic arterial hypotension.Recent data indicate that inhaled NO can be applied in various diseases. For example, studies suggest that inhaled NO is a safe and effective agent to determine the vasodilatory capacity of the pulmonary vascular bed. This article summarizes the pharmacology and physiology of inhaled NO and reviews the current uses of inhaled NO for the treatment, evaluation, and prevention of cardiovascular and respiratory diseases. Pharmacology and Physiology of Inhaled NO Chemistry of NO GasNO is a colorless, odorless gas that is only slightly soluble in water. 3 NO and its oxidative byproducts (eg, NO 2 and N 2 O 4 ) are produced by the partial oxidation of atmospheric nitrogen in internal combustion engines, in the burning cinder cones of cigarettes, and in lightning storms. Medical-grade NO gas is produced under carefully controlled conditions, diluted with pure nitrogen, and stored in the absence of oxygen. The recent article by Williams 4 provides a review of the chemistry of NO. Therapeutic Versus Endogenous NO Concentrations in the AirwayAlthough early studies of inhaled NO in the treatment of pulmonary hypertension used concentrations of 5 to 80 ppm, it has since been realized that concentrations Ͼ20 ppm provide little additional hemodynamic benefit in most patients. In some adults with acute respiratory failure, the effective concentrations of inhaled NO required to improve oxygenation can be as low as 10 ppb. 5,6 Of note, NO has been detected in exhaled human breath. The majority of exhaled NO in normal humans appears to be derived from nasal bacterial flora (25 to 64 ppb), with lower concentrations measured in the mouth, trachea, and distal airway (1 to 6 ppb). 5,7 Mechanism of ActionAfter inhalation, NO diffuses rapidly across the alveolarcapillary membrane into the subjacent smooth muscle of pulmonary vessels to activate soluble guanylate cyclase (Figure 1). This enzyme mediates many of the biological effects of NO and is responsible for the conversion of GTP to cGMP. Increased intracellular concentrations of cGMP relax smooth muscle via several mechanisms. The physiological actions of cGMP are limited to its area of synthesis by its hydrolysis to GMP by cyclic nucleotide phosphodiesterases (PDE) or by its export from the cell. Of the 11 reported...

show abstract

“…[2][3][4][5] In this report, we present the results of a blinded study designed to assess the efficacy of iNO 10 ppm on oxygenation, shunt, and pulmonary vascular resistance in severely hypoxemic, ventilated patients and to determine the optimal dose, in terms of improvement in PaO 2 , to five doses of iNO. PaO 2 ·FIO 2 -1 ratio <200 despite mechanical ventilation with 100% oxygen, and a mean PAP greater than 20 mmHg.…”

Section: Conclusion : Nos Résultats Indiquent Que L'ino Améliore L'oxmentioning

confidence: 99%

Rescue therapy with inhaled nitric oxide in critically ill patients with severe hypoxemic respiratory failure (Brief report)

Baxter

Randall

Miller

et al. 2002

Can J Anesth/J Can Anesth

View full text Add to dashboard Cite

Purpose: To evaluate the efficacy of inhaled nitric oxide (iNO) on oxygenation, shunt, and pulmonary vascular resistance index (PVRI) in severely hypoxemic, ventilated patients.Methods: In a two-period double-blind crossover design, 14 critically ill, hypoxemic, ventilated patients were randomized to receive iNO 10 ppm in 100% oxygen or no iNO in 100% oxygen for 30 min followed by a 30-min washout period and then crossed over to the other intervention. Responders to iNO then received iNO, which was increased from 5 ppm to 25 ppm in 5 ppm increments. Severity of illness scores and cardiorespiratory variables were measured.Results: Nitric oxide decreased shunt (P=0.002) and PVRI (P=0.033) and increased oxygenation (P=0.011) although the latter two were not statistically significant after adjustment for multiple comparisons. Treatment by period interactions were observed.Conclusion: Our findings suggest that iNO improves oxygenation to a clinically significant extent in critically ill patients who are severely hypoxemic.

show abstract

Inhalation of nitric oxide in acute lung injury: results of a European multicentre study

Abstract: Improvement of oxygenation by INO did not increase the frequency of reversal of ALI. Use of inhaled NO in early ALI did not alter mortality although it did reduce the frequency of severe respiratory failure in patients developing severe hypoxaemia.

Cited by 371 publications

References 18 publications

Predictors of Outcome in 216 Subjects With ARDS Treated With Inhaled Epoprostenol

Predictors of Outcome in 216 Subjects With ARDS Treated With Inhaled Epoprostenol

Inhaled Nitric Oxide

Rescue therapy with inhaled nitric oxide in critically ill patients with severe hypoxemic respiratory failure (Brief report)

Contact Info

Product

Resources

About