Hyperoxia and lung disease

CEDOT, São Paulo, Brazil.
Current opinion in pulmonary medicine (Impact Factor: 2.76). 10/1998; 4(5):300-4. DOI: 10.1097/00063198-199809000-00010
Source: PubMed


Experimental studies and few human reports demonstrate that hyperoxia increases the level of reactive oxygen-derived free radicals and that these substances can produce oxidative cellular injury. However, available data suggest that the human lung is more resistant to hyperoxic oxidative damage than previously expected and demonstrate that absorption atelectasis is the most frequently pulmonary effect of inhalation of a high inspired oxygen fraction. Practically, the therapeutic use of high inspired oxygen fractions is limited to patients with acute lung injury and severe hypoxemia. Recent studies demonstrated that ventilator-induced lung injury is a more important cause of pulmonary damage in these patients than hyperoxic toxicity. New protective ventilatory strategies are associated with increased survival.

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    • "As RMs may also have negative clinical effects, their use should be carefully considered if they cannot be used to guide treatment. For example , some manoeuvres require FiO 2 =100% (Schiller et al., 2003; Stahl et al., 2006) to ensure adequate arterial oxygenation , which could cause harm due to oxygen toxicity (Jackson, 1985; Carvalho et al., 1998; Kazzaz et al., 1996). "
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    ABSTRACT: Respiratory manoeuvres which from normal operation of the mechanical ventilator have been used to provide additional information to identify respiratory mechanics models, guide treatment, or provide more insight for clinicians. However, if the underlying respiratory mechanics are changed by a respiratory manoeuvre, then the application of respiratory manoeuvres may be significantly limited. This study identifies respiratory mechanics before and after super-syringe manoeuvres to investigate if the well-known super-syringe manouevre changes the underlying patient-specific respiratory mechanics. Thirty breaths before and after a super-syringe manouevre are analysed using a first order model for each of 16 patients. Median [IQR] absolute percentage changes in the median identified compliance and resistance distributions were 8.9% [2.1-16.8%] for compliance and 12.0% [3.5-19.3%] for resistance. 12 of 16 patients had significant changes in the distributions of compliance and 10 had significant changes in distribution of resistance (Wilcoxon ranksum test p<0.05). The magnitude and direction of the changes in parameters varied across patients. Some patients had very similar respiratory mechanics before and after the respiratory manouevre, others had large changes. Large changes in respiratory mechanics for some patients after a manoeuvre, limit the ability of using manoeuvres to guide treatment, as patients whose respiratory mechanics are greatly altered by respiratory manoeuvres cannot be known in advance. Therefore, consideration should be given to the potential clinical benefits and harms of respiratory manoeuvres before using them on patients.
    Full-text · Conference Paper · Aug 2015
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    • "High oxygen concentrations are indispensable for neonates with immature lungs to meet respiratory insuYciency. Hyperoxia and the underdeveloped anti-oxidative capacity in preterm lungs take injurious eVects especially to the alveolar epithelium (Anhoj et al. 2002; Carvalho et al. 1998; French et al. 1999; Gesche et al. 2011; Pagano and Barazzone-ArgiroVo 2003). Beside other signaling molecules, members of the Wbroblast growth factor family (FGFs) are key factors governing lung development (Bellusci et al. 1997; Cardoso and Lu 2006; White et al. 2006). "
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    ABSTRACT: Development of preterm infant lungs is frequently impaired resulting in bronchopulmoary dysplasia (BPD). BPD results from interruption of physiologic anabolic intrauterine conditions, the inflammatory basis and therapeutic consequences of premature delivery, including increased oxygen supply for air breathing. The latter requires surfactant, produced by alveolar type II (AT II) cells to lower surface tension at the pulmonary air:liquid interface. Its main components are specific phosphatidylcholine (PC) species including dipalmitoyl-PC, anionic phospholipids and surfactant proteins. Local antioxidative enzymes are essential to cope with the pro-inflammatory side effects of normal alveolar oxygen pressures. However, respiratory insufficiency frequently requires increased oxygen supply. To cope with the injurious effects of hyperoxia to epithelia, recombinant human keratinocyte growth factor (rhKGF) was proposed as a surfactant stimulating, non-catabolic and epithelial-protective therapeutic. The aim of the present study was to examine the qualification of rhKGF to improve expression parameters of lung maturity in newborn rats under hyperoxic conditions (85 % O(2) for 7 days). In response to rhKGF proliferating cell nuclear antigen mRNA, as a feature of stimulated proliferation, was elevated. Similarly, the expressions of ATP-binding cassette protein A3 gene, a differentiation marker of AT II cells and of peroxiredoxin 6, thioredoxin and thioredoxin reductase, three genes involved in oxygen radical protection were increased. Furthermore, mRNA levels of acyl-coA:lysophosphatidylcholine acyltransferase 1, catalyzing dipalmitoyl-PC synthesis by acyl remodeling, and adipose triglyceride lipase, considered as responsible for fatty acid supply for surfactant PC synthesis, were elevated. These results, together with a considerable body of other confirmative evidence, suggest that rhKGF should be developed into a therapeutic option to treat preterm infants at risk for impaired lung development.
    Full-text · Article · Oct 2012 · Histochemie
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    • "Normobaric hyperoxia is an alternative strategy that is generally welltolerated with fewer potential side effects (e.g. loss of pulmonary surfactant) when administered for <24 h (Matalon et al., 1982; Royston et al., 1990; Carvalho et al., 1998; Brock and Di Giulio, 2006); it is readily available, inexpensive and can be initiated by emergency medical personnel within minutes after stroke symptom onset. Although normobaric hyperoxia reduced infarct size in all experimental stroke studies (Flynn and Auer, 2002; Singhal et al., 2002a, b; Kim et al., 2005), human experience has been limited. "
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    ABSTRACT: Normobaric hyperoxia is under investigation as a treatment for acute ischaemic stroke. In experimental models, normobaric hyperoxia reduces cerebral ischaemic injury and improves functional outcome. The mechanisms of neuroprotection are still debated because, (i) inhalation of 100% O2 does not significantly increase total blood O2 content; (ii) it is not known whether normobaric hyperoxia increases O2 delivery to the severely ischaemic cortex because of its short diffusion distance; and (iii) hyperoxia may reduce collateral cerebral blood flow (CBF) to ischaemic penumbra because it can cause vasoconstriction. We addressed these issues using real-time two-dimensional multispectral reflectance imaging and laser speckle flowmetry to simultaneously and non-invasively determine the impact of normobaric hyperoxia on CBF and oxygenation in ischaemic cortex. Ischaemia was induced by distal middle cerebral artery occlusion (dMCAO) in normoxic (30% inhaled O2, arterial pO2 134 +/- 9 mmHg), or hyperoxic mice (100% inhaled O2 starting 15 min after dMCAO, arterial pO2 312 +/- 10 mmHg). Post-ischaemic normobaric hyperoxia caused an immediate and progressive increase in oxyhaemoglobin (oxyHb) concentration, nearly doubling it in ischaemic core within 60 min. In addition, hyperoxia improved CBF so that the area of cortex with < or =20% residual CBF was decreased by 45% 60 min after dMCAO. Furthermore, hyperoxia reduced the frequency of peri-infarct depolarizations (PIDs) by more than 60%, and diminished their deleterious effects on CBF and metabolic load. Consistent with these findings, infarct size was reduced by 45% in the hyperoxia group 2 days after 75 min transient dMCAO. Our data show that normobaric hyperoxia increases tissue O2 delivery, and that novel mechanisms such as CBF augmentation, and suppression of PIDs may afford neuroprotection during hyperoxia.
    Full-text · Article · Jul 2007 · Brain
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