Low levels of nitric oxide as contaminant in hospital compressed air

Lee, Kang H.; Tan, Patrick Seow Koon; Rico, Philippe; Delgado, Edgar; Kellum, John A.; Pinsky, Michael R.

doi:10.1097/00003246-199707000-00014

Cited by 18 publications

(7 citation statements)

References 9 publications

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“…These data extend the findings of our group and others in subjects with normal lungs to include patient groups in whom inhaled NO may be considered as a therapeutic option. Although these increases in PaO 2 are minimal from a clinical perspective, they are consistent with our previous studies in healthy ventilator-dependent adults [13] and children with acute lung injury [23]. Furthermore, as demonstrated in our prior study in children, all the gas exchange changes can be attributed solely to these minimal levels of inhaled NO, in that they were duplicated when NOfree gas at the same FiO 2 (equivalent to our steps A1 and A2) was supplemented with exogenous NO to these very low levels [23].…”

Section: Discussionsupporting

confidence: 92%

“…Furthermore, the end-inspiratory and end-expiratory NO levels reached new steady state values within 5 min of changing steps. Furthermore, we [13] and others [1,2,3] have shown that changes in oxygenation in response to changes in inspired NO levels in subjects with hypoxia occur rapidly and tend to remain constant over at least an hour.…”

Section: Study Limitationsmentioning

confidence: 67%

“…Furthermore, we have previously documented that inadvertent NO delivery due to contamination of hospital gas at levels parallel these ambient levels [12] and that ventilator-dependent subjects with normal lungs given inhaled NO between 2 ppb and 550 ppb demonstrate improved oxygenation [13]. Although this is an interesting observation, its clinical relevance is questionable.…”

Section: Introductionmentioning

confidence: 95%

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Nitric oxide contamination of hospital compressed air improves gas exchange in patients with acute lung injury

et al. 2002

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Section: Discussionsupporting

confidence: 92%

Section: Study Limitationsmentioning

confidence: 67%

Section: Introductionmentioning

confidence: 95%

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Nitric oxide contamination of hospital compressed air improves gas exchange in patients with acute lung injury

et al. 2002

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“…Supplementation of NO‐containing nasal air to these patients improves arterial oxygenation and reduces pulmonary vascular resistance (Lundberg et al, 1995c). In addition, Pinsky et al have shown that the hospital pressurized air may contain NO levels similar to those described earlier (6–500 ppb) which may consequently have effects on arterial oxygenation and pulmonary arterial pressure in mechanically ventilated patients (Lee et al, 1997; Pinsky et al, 1997; Lum et al, 1998; Tan et al, 2002). In another study, nostril widening with breathe easy nasal strips improved arterial oxygenation in spontaneously breathing patients, likely by enhancing ventilation through the nasal airways thereby increasing NO delivery from the nasal airways to the lungs (Herulf et al, 1999).…”

Section: No As An “Aerocrine” Messengersupporting

confidence: 56%

Nitric Oxide and the Paranasal Sinuses

Lundberg

2008

The Anatomical Record

116

104

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The discovery within the paranasal sinuses for the production of nitric oxide (NO) has altered the traditional explanations of sinus physiology. This review article reports the ongoing investigation of sinus physiology beginning with the discovery of NO gas production in the paranasal sinuses that occurred in 1995, and the impact that finding has had both in the basic science and clinical arenas. It was shown that healthy paranasal sinus epithelium expresses an inducible NO synthase that continuously generates large amounts of NO, a pluripotent gaseous messenger with potent vasodilating, and antimicrobial activity. This NO can be measured noninvasively in nasally exhaled breath. The role of NO in the sinuses is likely to enhance local host defense mechanisms via direct inhibition of pathogen growth and stimulation of mucociliary activity. The NO concentration in a healthy sinus exceeds those that are needed for antibacterial effects in vitro. In patients with primary ciliary dyskinesia (PCD) and in cystic fibrosis, nasal NO is extremely low. This defect NO generation likely contributes to the great susceptibility to chronic sinusitis in these patients. In addition, the low-nasal NO is of diagnostic value especially in PCD, where nasal NO is very low or absent. Intriguingly, NO gas from the nose and sinuses is inhaled with every breath and reaches the lungs in a more diluted form to enhance pulmonary oxygen uptake via local vasodilation. In this sense NO may be regarded as an ''aerocrine'' hormone that is produced in the nose and sinuses and transported to a distal site of action with every inhalation.

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“…Hospital compressed air is often contaminated with NO, which effects patients. Levels of 13-79 ppb and 2-550 ppb improve oxygenation in neonates [29] and adults [30], respectively. In a study by MOURGEON et al [15], it was shown that more than half of the maximal effect of inhaled exogenous NO on arterial oxygenation and pulmonary artery pressure in patients with ARDS was achieved at levels of 150 ppb.…”

Section: Inhaled Nitric Oxidementioning

confidence: 97%

Nasal and oral contribution to inhaled and exhaled nitric oxide: a study in tracheotomized patients

Törnberg¹,

Marteus²,

Schedin³

et al. 2002

European Respiratory Journal

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Nitric oxide (NO) is produced at different sites in the human airways and may have several physiological effects. Orally-produced NO seems to contribute to the levels found in exhaled air. Autoinhalation of nasal NO increases oxygenation and reduces pulmonary artery pressure in humans. The aim of this study was to measure the concentration and output of NO during nasal, oral and tracheal controlled exhalation and inhalation.Ten tracheotomized patients and seven healthy subjects were studied. The mean ¡ SEM fraction of exhaled NO from the nose, mouth and trachea was 56 ¡ 8, 14 ¡ 4 and 6 ¡ 1 parts per billion (ppb), respectively. During single-breath nasal, oral and tracheal inhalation the fraction of inhaled NO was 64 ¡ 14, 11 ¡ 3 and 4 ¡ 1, respectively. There was a marked flow dependency on nasal NO output in the healthy subjects, which was four-fold greater at the higher flow rates, during inhalation when compared to exhalation.There is a substantial contribution of nasal and oral nitric oxide during both inhalation and exhalation. Nasal nitric oxide output is markedly higher during inhalation, reaching levels similar to those that are found to have clinical effects in the trachea. These findings have implications for the measurement of nitric oxide in exhaled air and the physiological effects of autoinhaled endogenous nitric oxide.

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Low levels of nitric oxide as contaminant in hospital compressed air

Abstract: The low concentration of nitric oxide in hospital compressed air improves oxygenation in patients with normal lungs receiving mechanical ventilation.

Cited by 18 publications

References 9 publications

Nitric oxide contamination of hospital compressed air improves gas exchange in patients with acute lung injury

Nitric oxide contamination of hospital compressed air improves gas exchange in patients with acute lung injury

Nitric Oxide and the Paranasal Sinuses

Nasal and oral contribution to inhaled and exhaled nitric oxide: a study in tracheotomized patients

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