The Response to Varying Concentrations of Inhaled Nitric Oxide in Patients with Acute Respiratory Distress Syndrome

Lowson, Stuart M.; Rich, George F.; McArdle, Philip A.; Jaidev, Joe; Morris, Geoffrey N.

doi:10.1213/00000539-199603000-00026

Cited by 9 publications

(18 citation statements)

References 16 publications

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“…Similar findings have been reported in studies by PUYBASSET et al [12] and ADATIA et al [22]. NO doses of as little as 1-2 ppm have been shown to be sufficient for optimal treatment of pulmonary hypertension in ARDS patients [9][10][11]. In contrast with these, as well as with the present study, the optimal NO dose in terms of pulmonary vasodilation was found to be as high as 100 ppm by GERLACH et al [13].…”

Section: Discussionsupporting

confidence: 92%

“…The present study further confirms that low NO doses, i.e. in the 0.5-5 ppm range, progressively improve Pa,O 2 in ARDS patients [8][9][10][11][12]. In addition, the results indicate that the Pa,O 2 response to NO doses >5 ppm varies between patients.…”

Section: Discussionsupporting

confidence: 87%

“…The various patterns in Pa,O 2 response observed in the present study support previous discordant findings on the doseresponse curves of NO for Pa,O 2 in ARDS patients. Some studies indicate that the effect of NO on Pa,O 2 reaches a plateau at 5 ppm or even lower doses [9][10][11][12]. Other data show that high NO doses can even deteriorate the Pa,O 2 response [13].…”

Section: Discussionmentioning

confidence: 99%

“…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].…”

mentioning

confidence: 99%

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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: 92%

Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

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 biopsy lung specimens from patients with PPH, the greater the area of pulmonary artery media, the greater the changes in PAP induced by intravenous or oral vasodilator drugs [20]. The reduction of mPAP during NO inhalation was correlated with the level of mPAP without NO in ARDS [12,13,21], chronic obstructive pulmonary disease [22] and congenital heart disease [18], but not in PPH [3] and another group of ARDS [5]. The degree of response to inhaled NO was quite variable [1].…”

Section: Discussionmentioning

confidence: 99%

Correlation of inhaled nitric-oxide induced reduction of pulmonary artery pressure and vascular changes

Jiang

Maruyama²,

Yokochi³

et al. 2002

Eur Respir J

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The purpose of the present study was to determine the relationship between hypertensive pulmonary vascular remodelling and the changes in mean pulmonary artery pressure (mPAP) during low-dose nitric oxide (NO) inhalation.Rats were exposed to chronic hypobaric hypoxia (air at 50.5 kPa (380 mmHg), 10% oxygen, for 5-29 days) to induce chronic pulmonary hypertension (PH) with pulmonary vascular structural changes. After the chronic hypoxic exposure, the rats had an indwelling pulmonary artery catheter inserted and changes in mPAP with NO were correlated to morphometrical analysis of pulmonary vascular changes.All concentrations of inhaled NO (0.1-2.0 parts per million) reduced mPAP with a similar per cent reduction from baseline mPAP in PH rats, while no changes were observed in control rats. During NO inhalation in PH rats, the absolute value of the decrease in mPAP, but not per cent reduction in mPAP, significantly correlated with baseline mPAP, the percentage of muscularised arteries at the alveolar wall level and at the alveolar duct level, and the per cent medial wall thickness of muscularised arteries.In the chronic hypoxic pulmonary hypertension model, the severity of pulmonary vascular remodelling did not alter the reactivity of the pulmonary arteries to nitric oxide and might, in part, determine the magnitude of nitric-oxide induced absolute reduction in mean pulmonary artery pressure. In all conditions causing pulmonary hypertension (PH), vascular changes include new muscularisation of normally non-muscular peripheral pulmonary arteries and medial muscle hypertrophy of normally muscular arteries. Abnormal muscular pulmonary vasculature might have a heightened reactivity [1, 2], which may explain the effect of nitric oxide (NO) inhalation in hypertensive pulmonary disease, because NO dilates constricted pulmonary vasculature. Although inhaled NO can dilate these structurallyremodelled pulmonary arteries, the degree of response to inhaled NO was quite variable in patients with congenital heart disease [1], primary pulmonary hypertension (PPH) [3], limited scleroderma and isolated PH [4] and severe acute respiratory distress syndrome (ARDS) [5]. The differences in severity of pulmonary vascular structural changes might explain the differences in inhaled NO-induced reduction in pulmonary artery pressure (PAP) among patients.Chronic hypoxia induces PH and hypertensive pulmonary vascular changes in rats [6][7][8]. With increasing exposure to hypoxia, there is a progressive increase in the severity of the hypertensive pulmonary vascular changes [7]. These findings allowed the authors to make a rat model of experimentally different degrees of PH and hypertensive pulmonary vascular changes. To determine the relationship between the hypertensive pulmonary vascular changes and response to inhaled NO, NO inhalation was carried out in a rat model of chronic PH induced by chronic hypoxic exposure of varying durations. Quantitative morphometrical analysis was applied to determine the severity of hypertensive pu...

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Acute and sustained effects of early administration of inhaled nitric oxide to children with acute respiratory distress syndrome.

Fiorette¹,

Moreas²,

Bonatto³

et al. 2004

Pediatric Critical Care Medicine

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To determine the acute and sustained effects of early inhaled nitric oxide on some oxygenation indexes and ventilator settings and to compare inhaled nitric oxide administration and conventional therapy on mortality rate, length of stay in intensive care, and duration of mechanical ventilation in children with acute respiratory distress syndrome. Design: Observational study. Setting: Pediatric intensive care unit at a university-affiliated hospital. Patients: Children with acute respiratory distress syndrome, aged between 1 month and 12 yrs. Interventions: Two groups were studied: an inhaled nitric oxide group (iNOG, n ‫؍‬ 18) composed of patients prospectively enrolled from November 2000 to November 2002, and a conventional therapy group (CTG, n ‫؍‬ 21) consisting of historical control patients admitted from August 1998 to August 2000. Measurements and Main Results: Therapy with inhaled nitric oxide was introduced as early as 1.5 hrs after acute respiratory distress syndrome diagnosis with acute improvements in PaO 2 / FIO 2 ratio (83.7%) and oxygenation index (46.7%). Study groups were of similar ages, gender, primary diagnoses, pediatric risk of mortality score, and mean airway pressure. PaO 2 /FIO 2 ratio was

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The Response to Varying Concentrations of Inhaled Nitric Oxide in Patients with Acute Respiratory Distress Syndrome

Cited by 9 publications

References 16 publications

Acute effects of inhaled nitric oxide in adult respiratory distress syndrome

Acute effects of inhaled nitric oxide in adult respiratory distress syndrome

Correlation of inhaled nitric-oxide induced reduction of pulmonary artery pressure and vascular changes

Acute and sustained effects of early administration of inhaled nitric oxide to children with acute respiratory distress syndrome.

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