Lung surfactant components in bronchoalveolar lavage after inhalation of NO2 as markers of altered surfactant metabolism

Müller, Bernd; Schäfer, Heiner; Barth, Peter; Wichert, P. von

doi:10.1007/bf00185077

Cited by 33 publications

(15 citation statements)

References 24 publications

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“…The amount of saturated PC was decreased, and the amount of unsaturated PC was increased. These investigators also observed an impaired surfactant function [89]. Lower PC levels may be caused by a decreased production and secretion of disaturated PC as observed in rats exposed to 5 ppm NO 2 for 48 h [81].…”

Section: Nitrogen Dioxidementioning

confidence: 74%

Toxic oxidant species and their impact on the pulmonary surfactant system

Putman

Golde

Haagsman

1997

Lung

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In this review the effects of oxidant inhalation on the pulmonary surfactant system of laboratory animals are discussed. Oxidant lung injury is a complex phenomenon with many aspects. Inhaled oxidants interact primarily with the epithelial lining fluid (ELF), a thin layer covering the epithelial cells of the lung which contains surfactant and antioxidants. In the upper airways this layer is thick and contains high levels of antioxidants. Therefore oxidant injury in this area is rare and is more common in the lower airways where the ELF is thin and contains fewer antioxidants. In the ELF oxidants can react with antioxidants or biomolecules, resulting in inactivation of the biomolecules or in the formation of even more reactive agents. Oxidation of extracellular surfactant constituents may impair its function and affect breathing. Oxidized ELF constituents may promote inflammation and edema, which will impair the surfactant system further. Animal species differences in respiratory tract anatomy, ventilatory rate, and antioxidant levels influence susceptibility to oxidants. The oxidant exposure dose dictates injury, subsequent repair processes, and tolerance induction.

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Section: Nitrogen Dioxidementioning

confidence: 74%

Toxic oxidant species and their impact on the pulmonary surfactant system

Putman

Golde

Haagsman

1997

Lung

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“…Finally, NO 2 concentrations of 1.5 ppm increased granulocyte and macrophage recruitment in the lungs [25] and produced hypertrophy of alveolar septa after 6 weeks of NO 2 exposure [26]. Conversely, no significant alterations in the number of inflammatory cells, in phospholipid content and in functional properties of surfactant could be demonstrated after NO 2 exposures of 0.8 ppm for 3 days in lung lavage products from rat lungs [27]. In our study, no evidence of pulmonary inflammation or acute distal injury due to 20 ppm NO inhalation could be found.…”

Section: Discussionmentioning

confidence: 97%

Inhaled Nitric Oxide neither Alters Oxidative Stress Parameters nor Induces Lung Inflammation in Premature Lambs with Moderate Hyaline Membrane Disease

Storme¹,

Zerimech

Riou³

et al. 1998

Neonatology

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The purpose of this investigation was to examine whether inhaled nitric oxide (NO) may alter oxidative stress parameters and induce lung inflammation in moderate hyaline membrane disease (HMD). Eighteen moderately premature lambs (130 days gestation, term = 147 days) were randomly assigned to treatment with 20 ppm inhaled NO (n = 8) from the onset of ventilation or used as control (n = 10). Except inhaled NO, treatments were intentionally similar to those applied in clinical situations. The main studied parameters were oxidative stress index measurements on lung parenchyma and in circulating blood, lung parenchyma microscopic examination and bronchoalveolar lavage cell count. We found that 20 ppm of inhaled NO for 5 h did not change significantly either malondialdehyde and total antioxidant status levels in circulating blood, or malondialdehyde, reduced glutathione, glutathione peroxidase and glutathione reductase in lung parenchyma. Amino-imino-propene bond generation, which are lipoperoxidation markers, was similar in both groups. Furthermore, no significant changes in the number of inflammatory cells in lung lavage products and in lung parenchyma microscopic examination could be found. Therefore, these data do not support the hypothesis that short-term NO inhalation increases oxidative stress and lung inflammation in an experimental model of moderate HMD.

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“…Interestingly, in a model of acute lung injury from sepsis and hyperoxia, there was no difference in total surfactant levels or large aggregates in lavages between wild and inducible NOS (Ϫ/Ϫ) knockout mice (4). The conflicting results between in vivo and in vitro studies may be explained by the presence of various antioxidants within epithelial lining fluid in vivo not present in vitro, which inactivates the toxic intermediates of NO, such as peroxynitrite (26,27,29,43,60), methemoglobin (30,31,33), and nitrogen dioxide (45), which affect SP synthesis, secretion, or function.…”

Section: Discussionmentioning

confidence: 99%

Increased pulmonary blood flow does not alter surfactant protein gene expression in lambs within the first week of life

Lee¹,

Ovadia²,

Azakie³

et al. 2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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Neonates and infants with congenital heart disease with increased pulmonary blood flow suffer morbidity from poor oxygenation and decreased lung compliance. In a previous experiment involving 4-wk-old lambs with pulmonary hypertension secondary to increased pulmonary blood flow following an in utero placement of an aortopulmonary vascular graft, we found a decrease in surfactant protein (SP)-A gene expression as well as a decrease in SP-A and SP-B protein contents. To determine the timing of these changes, the objective of the present study was to characterize the effect of increased pulmonary blood flow and pulmonary hypertension on SP-A, -B, and -C gene expressions and protein contents within the first week of life. Of eight fetal lambs that underwent the in utero placement of the shunt, there was no difference in the expression of SP-A, -B, and -C mRNA levels or SP-A and -B protein contents compared with age-matched controls. The results showed that, in this model of congenital heart disease with pulmonary hypertension and increased pulmonary blood flow, the effect of the shunt on SP gene expression and protein content was not apparent within the first week of life.congenital heart disease AMONG NEONATES AND INFANTS with congenital heart disease with increased pulmonary blood flow, the presence of the systemicto-pulmonary communication often leads to progressive structural and functional changes in the pulmonary vascular bed, leading to pulmonary hypertension. The structural changes include increased muscularity of small pulmonary arteries with early distal extension, intimal hyperplasia, scarring and thrombosis, and a reduction in the number of intra-acinar arteries, as well as the arterial-to-alveolar ratio. These vascular changes result in eventual obliteration of the pulmonary vascular bed with elevation in pulmonary vascular resistance and extreme sensitivity to vasoconstricting stimuli. If uncorrected, these children will suffer from morbidity from cyanosis and myocardial failure (12,34,49).Multiple studies have shown that increased pulmonary blood flow and/or pressure affect endothelial cell functions within the alveolar space. Grigg et al. (22) found elevated levels of endothelin-1 (ET-1) in bronchoalveolar lavage in children with congenital heart disease with increased pulmonary blood flow. Ishikawa et al. (36) found elevated plasma ET-1 levels in children with ventricular septal defects who had both volume and pressure overload to the pulmonary circulation but not in children with atrial septal defects who had only volume overload. In cultured human vascular endothelial cells, shear stress stimulated the synthesis of mRNA for platelet-derived growth factors-A and -B (48), tissue plasminogen activator (20), and intercellular adhesion molecule-1 (46).Recently, increased pulmonary blood flow and/or pressure has also been shown to affect pulmonary epithelial cell functions. Wang et al. (59) showed that, in an isolated, constantly inflated, blood-perfused rat lung, increased left atrial pressure increa...

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Lung surfactant components in bronchoalveolar lavage after inhalation of NO2 as markers of altered surfactant metabolism

Cited by 33 publications

References 24 publications

Toxic oxidant species and their impact on the pulmonary surfactant system

Toxic oxidant species and their impact on the pulmonary surfactant system

Inhaled Nitric Oxide neither Alters Oxidative Stress Parameters nor Induces Lung Inflammation in Premature Lambs with Moderate Hyaline Membrane Disease

Increased pulmonary blood flow does not alter surfactant protein gene expression in lambs within the first week of life

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