Pulmonary Effects of Oxygen Breathing a 6-Hour Study in Normal Men

Sackner, Marvin A.; Landa, Jose; Hirsch, Judith A.; Zapata, Á. Lancharro

doi:10.1097/00132586-197602000-00001

Cited by 19 publications

(24 citation statements)

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“…Hyperoxia leads to oxidant injury in the respiratory tract, which is manifest as acute tracheobronchitis with edema and decrease in mucocili-(Received in original form July 8, 2005 and in final form May 4, 2006 ) This study was supported by AI70649, HL60917, and M01 RR018390 from the National Center for Research Resources. A.C. was supported by grants from the Collège des Professeurs de Pneumologie.Correspondence and requests for reprints should be addressed to Serpil C. (12,13). Oxidative damage of proteins and loss of biological function is one defined end-point of hyperoxic injury (1,(5)(6)(7)(8).…”

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confidence: 99%

“…Correspondence and requests for reprints should be addressed to Serpil C. (12,13). Oxidative damage of proteins and loss of biological function is one defined end-point of hyperoxic injury (1,(5)(6)(7)(8).…”

mentioning

confidence: 99%

“…The bronchial epithelium is particularly vulnerable to the effects of airborne oxidative stress as the moist mucosal surface of the airway is in direct contact with the environment (11). Hyperoxia leads to oxidant injury in the respiratory tract, which is manifest as acute tracheobronchitis with edema and decrease in mucocili-ary clearance (12,13). Oxidative damage of proteins and loss of biological function is one defined end-point of hyperoxic injury (1,(5)(6)(7)(8).…”

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confidence: 99%

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Gene Expression Profile of Human Airway Epithelium Induced by Hyperoxia In Vivo

Chambellan

Cruickshank²,

McKenzie³

et al. 2006

Am J Respir Cell Mol Biol

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Hyperoxia leads to oxidative modification and damage of macromolecules in the respiratory tract with loss of biological functions. Given the lack of antioxidant gene induction with acute exposure to 100% oxygen, we hypothesized that clearance pathways for oxidatively modified proteins may be induced and serve in the immediate cellular response to preserve the epithelial layer. To test this, airway epithelial cells were obtained from individuals under ambient oxygen conditions and after breathing 100% oxygen for 12 h. Gene expression profiling identified induction of genes in the chaperone and proteasome-ubiquitin-conjugation pathways that together comprise an integrated cellular response to manage and degrade damaged proteins. Analyses also revealed gene expression changes associated with oxidoreductase function, cell cycle regulation, and ATP synthesis. Increased HSP70, protein ubiquitination, and intracellular ATP were validated in cells exposed to hyperoxia in vitro. Inhibition of proteasomal degradation revealed the importance of accelerated protein catabolism for energy production of cells exposed to hyperoxia. Thus, the human airway early response to hyperoxia relies predominantly upon induction of cytoprotective chaperones and the ubiquitin-proteasome-dependent protein degradation system to maintain airway homeostatic integrity.Keywords: airways; gene expression; hyperoxia; proteasome; ubiquitin Oxygen, one of the most abundant elements in our world, is essential for the oxidation of organic compounds to generate the energy needed to sustain life. Under ambient conditions, reactive oxygen species (ROS) are generated at a low level in lung cells during aerobic metabolism. To minimize the oxidant injury that is a consequence of aerobic life, the human lung is endowed with an integrated antioxidant system, which detoxifies reactive products (1-4). However, excessive ROS may overwhelm the antioxidant system and result in damage to major cellular components, including membrane lipids, proteins, carbohydrates, and DNA (1,(5)(6)(7)(8). The pathophysiologic consequences of this injury may include cell death, and tissue inflammation and damage. This is particularly evident during conditions of increased oxygen exposure for medical therapy (4, 9, 10). The bronchial epithelium is particularly vulnerable to the effects of airborne oxidative stress as the moist mucosal surface of the airway is in direct contact with the environment (11). Hyperoxia leads to oxidant injury in the respiratory tract, which is manifest as acute tracheobronchitis with edema and decrease in mucocili-(Received in original form July 8, 2005 and in final form May 4, 2006 ) This study was supported by AI70649, HL60917, and M01 RR018390 from the National Center for Research Resources. A.C. was supported by grants from the Collège des Professeurs de Pneumologie.Correspondence and requests for reprints should be addressed to Serpil C. (12,13). Oxidative damage of proteins and loss of biological function is one defined end-point of hyperoxic inj...

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Gene Expression Profile of Human Airway Epithelium Induced by Hyperoxia In Vivo

Chambellan

Cruickshank²,

McKenzie³

et al. 2006

Am J Respir Cell Mol Biol

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“…Sackner et al reported that erythema and edema of the large airways can be observed bronchoscopically in the majority of patients treated with a FiO2 of 90% for six hours and this is thought to reflect hyperoxic bronchitis (22). In a study by Freeman et al normobaric oxygen therapy with 85% oxygen continuously for 7 days, resulted in lung toxicity in rats (17).…”

Section: Discussionmentioning

confidence: 99%

Histologic Evaluation of Normobaric Oxygen Therapy Safety in an Animal Model

Idani

Ranjbari

Sharifipour

et al. 2012

Jundishapur J Nat Pharm Prod

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“…High level of FiO 2 is responsible for denitrogenation phenomena and inhibition of surfactant production promoting expiratory collapse and atelectasis (21)(22)(23). Adsorption atelectasis occurs within few minutes after pure O 2 breathing (23)(24)(25).…”

Section: Experimental Studiesmentioning

confidence: 99%

Relationship between hyperoxemia and ventilator associated pneumonia

et al. 2017

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Previous studies suggest a relationship between hyperoxemia and ventilator-associated pneumonia (VAP). Hyperoxemia is responsible for denitrogenation phenomena, and inhibition of surfactant production, promoting atelectasis in mechanically ventilated patients. Further, hyperoxemia impairs the efficacy of alveolar macrophages to migrate, phagocyte and kill bacteria. Oxygen can also cause pulmonaryspecific toxic effect called hyperoxic acute lung injury leading to longer duration of mechanical ventilation.All these hyperoxic effects are well-known risk factors for VAP. A recent retrospective large single center study identified hyperoxemia as an independent risk factor for VAP. However, two recent randomized controlled trials evaluated the impact of conservative oxygen strategy versus a liberal strategy, but did not confirm the role of hyperoxemia in lower respiratory tract infection occurrence. In this review, we discuss animal and human studies suggesting a relationship between these two common conditions in mechanically ventilated patients and potential interventions that should be evaluated. Further large prospective studies in carefully selected groups of patients are required to confirm the potential role of hyperoxemia in VAP pathogenesis and to evaluate the impact of a conservative oxygen strategy vs. a conventional strategy on the incidence of VAP.

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Pulmonary Effects of Oxygen Breathing a 6-Hour Study in Normal Men

Cited by 19 publications

References 0 publications

Gene Expression Profile of Human Airway Epithelium Induced by Hyperoxia In Vivo

Gene Expression Profile of Human Airway Epithelium Induced by Hyperoxia In Vivo

Histologic Evaluation of Normobaric Oxygen Therapy Safety in an Animal Model

Relationship between hyperoxemia and ventilator associated pneumonia

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