On-line measurement of nitric oxide generation in buffer-perfused rabbit lungs

Spriestersbach, R.; Grimminger, Friedrich; Weißmann, Norbert; Walmrath, D.; Seeger, W.

doi:10.1152/jappl.1995.78.4.1502

Cited by 36 publications

(33 citation statements)

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“…The technique of exhaled and perfusate NO levels has been previously described (28). In brief, an aliquot of the mixed expired gas was continuously forwarded to a chemiluminescence NO analyzer (280 NOA; Sievers Instruments, Boulder, CO) to measure exhaled NO concentration.…”

Section: Methodsmentioning

confidence: 99%

“…In brief, an aliquot of the mixed expired gas was continuously forwarded to a chemiluminescence NO analyzer (280 NOA; Sievers Instruments, Boulder, CO) to measure exhaled NO concentration. For determination of NO concentrations released into the buffer fluid, samples were taken every 25 min and analyzed as described before (28).…”

Section: Methodsmentioning

confidence: 99%

“…Few studies have addressed the role of nitric oxide (NO), which is known as a highly important factor in hypoxic pulmonary vascular reactivity, for hypercapnia and/or acidosis on HPV and pulmonary vascular resistance (28,37). Nevertheless, some investigators found a decrease in NO production caused by hypercapnia (1,29,42), and others describe an increase (15,41,44).…”

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confidence: 99%

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Effects of hypercapnia with and without acidosis on hypoxic pulmonary vasoconstriction

Ketabchi

Egemnazarov²,

Schermuly³

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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Acute respiratory disorders and permissive hypercapnic strategy may lead to alveolar hypoxia and hypercapnic acidosis. However, the effects of hypercapnia with or without acidosis on hypoxic pulmonary vasoconstriction (HPV) and oxygen diffusion capacity of the lung are controversial. We investigated the effects of hypercapnic acidosis and hypercapnia with normal pH (pH corrected with sodium bicarbonate) on HPV, capillary permeability, gas exchange, and ventilation-perfusion matching in the isolated ventilated-perfused rabbit lung. No alteration in vascular tone was noted during normoxic hypercapnia with or without acidosis compared with normoxic normocapnia. Hypercapnia with normal pH resulted in a transient increase in HPV during the course of consecutive ventilation maneuvers, whereas hypercapnic acidosis increased HPV over time. Hypercapnic acidosis decreased exhaled NO during hypoxia more than hypercapnia with normal pH and normocapnia, whereas intravascular NO release was unchanged. However, inhibition of NO synthesis by nitro-L-arginine (L-NNA) resulted in a loss of the increased HPV caused by hypercapnic acidosis but not that caused by hypercapnia with normal pH. Furthermore, capillary permeability increased during hypoxic hypercapnia with normal pH but not hypoxic hypercapnic acidosis. This effect was NO-dependent because it disappeared during L-NNA administration. Ventilation-perfusion matching and arterial PO2 were improved according to the strength of HPV in hypercapnia compared with normocapnia during Tween nebulization-induced lung injury. In conclusion, the increased HPV during hypercapnic acidosis is beneficial to lung gas exchange by improving ventilation-perfusion matching and preserving the capillary barrier function. These effects seem to be linked to NO-mediated pathways.hypoxia; hypercapnic acidosis; pH; capillary permeability ACUTE RESPIRATORY DISORDERS such as acute obstructive pulmonary diseases and depression of the respiratory control center may induce alveolar hypoxia and hypercapnic acidosis, which can affect systemic regulatory processes and pulmonary function. However, the use of sodium bicarbonate, one of the most essential extracellular buffers for the normalization of pH in different pathological conditions of respiratory acidosis, is controversial. During resuscitation, application of sodium bicarbonate is generally not recommended for just correction of pH due to severe side effects (40). Furthermore, in permissive hypercapnic strategy, beneficial effects of acidosis have been discussed in the literature (5). In animal studies, a decreased development of pulmonary edema and reduced hypoxemia during hypercapnic acidosis suggests valuable effects of acidosis (13,14,(25)(26)(27), whereas from other studies it could not be distinguished whether the effects were related to hypercapnia or acidosis (12,43). In addition, the mechanisms of improvement of oxygenation and reduced lung edema formation are not known. Improvement in ventilation-perfusion matching and/or of gas diffusion acro...

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Effects of hypercapnia with and without acidosis on hypoxic pulmonary vasoconstriction

Ketabchi

Egemnazarov²,

Schermuly³

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Due to the very low liquid-gas partition coefficient of NO, NO released into the culture medium is expected to largely escape into the gaseous headspace (25).…”

Section: Measurement Of Cellular No Releasementioning

confidence: 99%

Apical, But Not Basolateral, Endotoxin Preincubation Protects Alveolar Epithelial Cells Against Hydrogen Peroxide-Induced Loss of Barrier Function: The Role of Nitric Oxide Synthesis

Rose

Guthmann

Tenenbaum

et al. 2002

The Journal of Immunology

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The influence of LPS preincubation on hydrogen peroxide (H2O2)-induced loss of epithelial barrier function was investigated in rat alveolar epithelial type II cells (ATII). Both apical and basolateral H2O2 administration caused a manyfold increase in transepithelial [3H]mannitol passage. Apical but not basolateral preincubation of ATII with LPS did not influence control barrier properties but fully abrogated the H2O2-induced leakage response. The effect of apical LPS was CD14 dependent and was accompanied by a strong up-regulation of NO synthase II mRNA and protein and NO release. Inhibition of NO by NG-monomethyl-l-arginine suppressed the LPS effect, whereas it was reproduced by exogenous application of gaseous NO or NO donor agents. Manipulation of the glutathione homeostasis (buthionine-(S,R)-sulfoximine) and the cGMP pathway (1H-(1,2,4)oxadiazolo[4,3-α]quinoxaline-1-one; zaprinast) did not interfere with the protective effect of LPS. Superoxide (O⨪2) generation by ATII cells was reduced by exogenous NO and LPS preincubation. O⨪2 scavenging with exogenous superoxide dismutase, the intracellular superoxide dismutase analog Mn(III)tetrakis(4-benzoic acid) porphyrin, and the superoxide scavenger nitroblue tetrazolium and, in particular, hydroxyl radical scavenging with hydroxyl radical scavenger 1,3-dimethyl-thiourea inhibited the H2O2-induced epithelial leakage response. In conclusion, apical but not basolateral LPS preincubation of ATII cells provides strong protection against H2O2-induced transepithelial leakage, attributable to an up-regulation of epithelial NO synthesis. It is suggested that the LPS-induced NO formation is effective via interaction with reactive oxygen species, including superoxide and hydroxyl radicals. The polarized epithelial response to LPS may be part of the lung innate immune system, activated by inhaled endotoxin or under conditions of pneumonia.

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“…NO has several physiological functions. It contributes to the modulation of the pulmonary vascular tone under physiological conditions and, perhaps more importantly, during hypoxia [1]. The major portion of endogenous NO is produced in the upper respiratory tract, particularly in the nasopharynx [2][3][4].…”

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confidence: 99%

Replacement of physiologically autoinhaled nitric oxide in intubated patients

Röhrig

Kuhlen²,

Baumert³

et al. 2003

Eur Respir J

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Autoinhaled nitric oxide (NO) is produced mainly in the upper airways. Orotracheal intubation disrupts the natural autoinhalation of NO from the naso-and oropharynx. The effect of disrupting and then replacing autoinhaled NO on arterial oxygenation was investigated in intubated patients.Two groups of nine patients without lung disease were examined during anaesthesia using an inspired oxygen fraction of 0.50. In both groups, the individually produced NO of the whole respiratory tract and the upper airways was determined. The amount of NO normally autoinhaled from the upper airways was replaced for 5 min after orotracheal intubation in one group.The amount of NO from the upper respiratory tract was 47¡19 parts per billion (ppb) in the test group and the replaced NO concentration was 48¡20 ppb. No significant increase in arterial oxygen tension could be detected during the replacement of the autoinhaled NO. Haemodynamic parameters remained unchanged. In the control group, the NO from the upper airways was 34¡16 ppb. In contrast to the test group, it was not replaced after intubation.These findings suggest that in healthy subjects the autoinhalation of nitric oxide does not play an important role in arterial oxygenation during anaesthesia. Nitric oxide (NO) is formed within the respiratory tract by the enzyme NO synthase, which converts L-arginine to L-citrulline. NO has several physiological functions. It contributes to the modulation of the pulmonary vascular tone under physiological conditions and, perhaps more importantly, during hypoxia [1]. The major portion of endogenous NO is produced in the upper respiratory tract, particularly in the nasopharynx [2][3][4]. Under physiological conditions the NO produced in the oro-and nasopharynx is inhaled to some extent. Endotracheal intubation disrupts this autoinhalation from the upper airways. It is estimated that y50-100 parts per billion (ppb) are autoinhaled during normal breathing [2,5]. In various diseases associated with pulmonary hypertension, inhalation of exogenous NO in supranormal concentrations is used as a therapeutic means to selectively decrease pulmonary vascular resistance in ventilated lung regions. Therefore, the ventilation/perfusion mismatch and the intrapulmonary right-to-left shunt are reduced, and consequently the arterial oxygenation is improved [6][7][8][9][10]. The physiological implication of autoinhaled NO in healthy humans is still unknown.Bypassing the upper airway by orotracheal intubation disrupts the autoinhalation of NO from the oro-and nasopharynx. Therefore, the authors sought to investigate the physiological role of autoinhaled NO in patients in whom anaesthesia was induced and who were intubated. The hypothesis that the replacement of the exact amount of endogenous NO influences the arterial oxygenation was tested in a randomised, controlled study. MethodsThe study was approved by the hospital ethics committee and informed consent was obtained from each patient the day prior to the operation. PatientsThe patients invest...

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On-line measurement of nitric oxide generation in buffer-perfused rabbit lungs

Cited by 36 publications

References 0 publications

Effects of hypercapnia with and without acidosis on hypoxic pulmonary vasoconstriction

Effects of hypercapnia with and without acidosis on hypoxic pulmonary vasoconstriction

Apical, But Not Basolateral, Endotoxin Preincubation Protects Alveolar Epithelial Cells Against Hydrogen Peroxide-Induced Loss of Barrier Function: The Role of Nitric Oxide Synthesis

Replacement of physiologically autoinhaled nitric oxide in intubated patients

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