Effects of inhaled nitric oxide on right ventricular function in severe acute respiratory distress syndrome

Rossaint, Rolf; Slama, K.; Steudel, Wolfgang; Gerlach, Herwig; Pappert, D.; Veit, S; Falke, K. J.

doi:10.1007/bf01701472

Cited by 116 publications

(34 citation statements)

References 31 publications

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“…Potentially, inhaled NO can increase DO 2 by two mechanisms: through increases in Ca,O 2 and through increases in CI. Clinically relevant increases in CI are induced by inhaled NO only when right ventricular function is severely impaired, which is a rare event in ARDS patients [27,28]. The present study further confirms that normally, in ARDS patients, inhaled NO does not significantly affect CI, while the benefit of inhaled NO on DO 2 depends entirely on increased Ca,O 2 .…”

Section: Discussionsupporting

confidence: 83%

Acute effects of inhaled nitric oxide in adult respiratory distress syndrome

Iotti¹,

Olivei²,

Palo³

et al. 1998

Eur Respir J

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In patients with adult respiratory distress syndrome (ARDS), inhaled nitric oxide (NO) may both reduce pulmonary hypertension and improve arterial oxygenation [1,2]. The NO-induced decrease in pulmonary artery pressure depends on the selective pulmonary vasodilating effect of inhaled NO [3], while the NO-induced increase in arterial oxygenation is related to the redistribution of pulmonary blood flow to well-ventilated lung areas, which results in improved ventilation to perfusion matching [1,4]. Although potentially beneficial, inhaled NO is a toxic compound, and its toxicity is increased by the oxidation of NO to NO 2 , which occurs during administration of inhaled NO, especially when the inhaled oxygen concentration is high [5]. In order to minimize the risks of toxicity, inhaled NO should be administered at the lowest effective concentration to achieve maximal therapeutic effects [6,7].There is conflicting information on the NO dose for optimal treatment of pulmonary hypertension and hypoxaemia in ARDS. It has been shown that very low NO doses (<1 parts per million (ppm)) may have a measurable effect both on pulmonary circulation and on arterial oxygenation in ARDS patients [8][9][10]. Published data indicate that low NO doses, between 1-5 ppm, achieve maximal haemodynamic and oxygenation responses [9][10][11][12]. However, other studies in ARDS patients indicate that higher NO doses may induce an additional reduction in pulmonary hypertension and hypoxaemia. In a study by GERLACH et al. [13], a dose of NO as high as 100 ppm was required to achieve maximal pulmonary vasodilation, while the impro-vement in arterial oxygen tension (Pa,O 2 ) was maximal at 1 ppm. In contrast, a study on septic ARDS patients rep-orted a dose-dependent increase in Pa,O 2 in the range 0.1-150 ppm and a plateau effect in pulmonary pressure at 5 ppm [14]. A recent study showed that the optimum NO dose to improve Pa,O 2 may vary widely between individuals, ranging 0.1-100 ppm [15]. In that same study, however, the effect on pulmonary haemodynamics was negligible.The aim of this study was to evaluate the dose-response effect of inhaled NO (0.5-100 ppm) on gas exchange and haemodynamics in ARDS patients treated with conventional mechanical ventilation. Materials and methods PatientsDuring a 10-month period, 19 consecutive patients who were mechanically ventilated for severe ARDS were screen- Olivei, A. Palo, C. Galbusera, R. Veronesi, A. Braschi. ©ERS Journals Ltd 1998. ABSTRACT: This study evaluated the dose-response effect of inhaled nitric oxide (NO) on gas exchange, haemodynamics, and respiratory mechanics in patients with adult respiratory distress syndrome (ARDS). Acute effects of inhaled nitric oxide in adult respiratory distress syndrome. G.A. Iotti, M.C.Of 19 consecutive ARDS patients on mechanical ventilation, eight (42%) responded to a test of 10 parts per million (ppm) NO inhalation with a 25% increase in arterial oxygen tension (Pa,O 2 ) over the baseline value. The eight NO-responders were extensively studied during admin...

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Section: Discussionsupporting

confidence: 83%

Acute effects of inhaled nitric oxide in adult respiratory distress syndrome

Iotti¹,

Olivei²,

Palo³

et al. 1998

Eur Respir J

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“…36 ppm nur 0,1 ppm) [140]. Nachweisbar günstige Effekte auf den rechten Ventrikel fanden sich zunächst nur in wenigen Fällen [155]. Grund hierfür dürfte sein, dass die mit ARDS assoziierte pulmonale Hypertension meist moderat ist (mittlerer PAP um 30 mmHg) und nicht regelhaft eine rechtsventrikuläre Dysfunktion induziert.Liegt jedoch bei beatmeten Patienten (ARDS,COPD) eine manifeste Dilatation des rechten Ventrikels vor (dies ist bei ca.…”

Section: Ardsunclassified

Inhalierte Vasodilatatoren

Zwißler¹

2002

Anaesthesist

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First reports on the use of inhaled nitric oxide (NO) in patients were published in 1991. These reports confirmed data from animal experiments which suggested a selective vasodilatory effect of inhaled NO in pulmonary vessels. As the main clinical effects, both improved oxygenation and a drop of pulmonary artery pressure despite unchanged arterial pressure were observed. Since then, many studies have evaluated the effects of inhaled NO as well as of other aerosolised vasodilators (e.g. PGI(2), PGE(1), nitrates, phosphodiesterase-inhibitors) in patients with pulmonary hypertension, acute right heart failure and/or life-threatening hypoxemia. However, primary pulmonary hypertension of the newborn (PPHN) is the only indication for which inhaled NO has been clinically approved so far. Although an obvious clinical benefit in outcome from inhaled vasodilators has never been formally documented, good clinical efficacy has resulted in an increasing "off label" use of the concept both in Germany and worldwide, particularly with respect to anaesthesia and intensive care medicine. The present article aims to review both the pathophysiological and pharmacological basis of inhaled vasodilators, to critically reevaluate their potential clinical indications and to give a perspective on future developments in the field.

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“…Following the first ACH challenge test, the animals inhaled nebulized L-NAME solution at a concentration of 1.2 mM [23] for 40 min. The aerosols were generated by the nebulizer used for ACH aerosol generation.…”

Section: Influence Of No Synthase (Nos) Inhibitor L-name On Ar To Achmentioning

confidence: 99%

“…NO has many clinical applications including the normalization of pulmonary vascular pressure in newborns with severe persistent hypertension [10,20] and in the treatment of adult respiratory distress syndrome (ARDS) [6,18,22,23]. In addition, it serves as vasodilator in chronic obstructive pulmonary disease [21].…”

Section: Introductionmentioning

confidence: 99%

Modulation of Airway Responsiveness to Acetylcholine by Nitric Oxide in a Rabbit Model

Mensing

Marek

Baur

1997

Lung

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Nitric oxide (NO) is an important mediator in the regulation of bronchial muscle tone and airway responsiveness. We investigated the influence of exogenous NO on airway responsiveness to acetylcholine aerosols (ACH) in normal and in hyperresponsive rabbits. White New Zealand rabbits were anesthetized, intubated, and breathed room air spontaneously. Responses of respiratory parameters in ACH challenge tests were measured. In group A the influence of NO on ACH infusion-induced airway constriction was measured. Airway responses to aerosols from 0.25 to 8.0% ACH solutions in saline were measured with 150 and 300 ppm NO inhalation (groups B and C) and compared with the same animals' responses without NO. Moreover, we examined the influence of NO synthase inhibition on airway responsiveness (group D) and the modulatory effect of NO in hyperresponsive animals (group E). 300 ppm NO inhalation significantly decreased the bronchoconstrictor response to intravenously administered ACH (group A). However, the baseline value of dynamic elastance (Edyn) was only marginally lower under the influence of 300 ppm NO. During inhalation of 150 or 300 ppm NO, responses to nebulized 2.0% and less ACH solutions remained nearly unaltered. Responses to aerosols of 4.0 and 8.0% diminished significantly (groups B and C). Following 40 min of aerosolized N-nitro-L-arginine-methyl ester (L-NAME) solution (a NO synthase inhibitor, 1.2 mM) inhalation, the response of Edyn to ACH increased significantly in group D. In group E, animals inhaled 500 mg/m3 ammonium persulfate (APS), an oxidant with various industrial applications, after the first ACH challenge test (0.2, 1.0, and 2.0% ACH). After 2 h of APS exposure, the ACH-induced broncho constriction was increased significantly in the challenge test. After another 2 h of APS inhalation, the airway responsiveness to ACH was tested under the influence of 300 ppm NO. NO significantly decreased the response to ACH to almost the same level as before APS exposure. The results indicate that responses to high ACH concentrations as well as an APS-induced increase in ACH responsiveness were effectively reduced by high concentrations of inhaled NO.

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Effects of inhaled nitric oxide on right ventricular function in severe acute respiratory distress syndrome

Cited by 116 publications

References 31 publications

Acute effects of inhaled nitric oxide in adult respiratory distress syndrome

Acute effects of inhaled nitric oxide in adult respiratory distress syndrome

Inhalierte Vasodilatatoren

Modulation of Airway Responsiveness to Acetylcholine by Nitric Oxide in a Rabbit Model

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