On the Pulmonary Toxicity of Oxygen I. The Relationship of Oxygen Content to the Effect of Oxygen on the Lung

Shanklin, Douglas R.; Fairley, H. Barrie

doi:10.1097/00132586-197106000-00003

Cited by 8 publications

(43 citation statements)

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“…Animals were removed after death and were autopsied according to the methods and procedures previously reported (Shanklin and Berman, 1964;Shanklin and Sotelo-Avila, 1967;Shanklin, 1969). In brief, the extent of lesion was determined by a grid approximation .formula on the pleural surface of the lungs, with each of the four principal lobes considered separately.…”

Section: Methodsmentioning

confidence: 99%

“…Assignment of animals from given litters to a group was as before, with special attention to large litters and by weight (Shanklin, 1969). The sex ratio of individual groups was left to random sort by the minimum test group size as noted above (Shanklin and Berman, 1964;Shanklin and SoteloAvila, 1967;Shanklin, 1969) since the sex of the newborn animal is readily determined only at autopsy.…”

Section: Thyrotropinmentioning

confidence: 99%

“…The sex ratio of individual groups was left to random sort by the minimum test group size as noted above (Shanklin and Berman, 1964;Shanklin and SoteloAvila, 1967;Shanklin, 1969) since the sex of the newborn animal is readily determined only at autopsy.…”

Section: Thyrotropinmentioning

confidence: 99%

“…Earlier work from this laboratory demonstrated a complex but systematic relationship between the amount of oxygen to which the lung was exposed and the extent and severity of lung injury in a neonatal animal model for hyaline membrane disease (Shanklin, 1969;Shanklin and Lester, 1972). The model is based on the effects of bilateral cervical vagotomy (BCV) on the lung (Farber, 1937).…”

Section: Introductionmentioning

confidence: 99%

“…These experiments used oxygen at 7, 21, 40, and 60 percent against nitrogen, and at 1 00% oxygen in hypobaric (0.2 and 0.6 ATA), normobaric, and hyperbaric (3.0 ATA) total pressure (Shanklin, 1969).…”

Section: Introductionmentioning

confidence: 99%

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On the pulmonary toxicity of oxygen. 4. The thyroid arena

Shanklin

2012

Experimental and Molecular Pathology

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Section: Methodsmentioning

confidence: 99%

Section: Thyrotropinmentioning

confidence: 99%

Section: Thyrotropinmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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On the pulmonary toxicity of oxygen. 4. The thyroid arena

Shanklin

2012

Experimental and Molecular Pathology

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On the pulmonary toxicity of oxygen: III. The induction of oxygen dependency by oxygen use

Shanklin

2010

Experimental and Molecular Pathology

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Oxygen is central to the development of neonatal lung injury. The increase in oxygen exposure of the neonatal lung during the onset of extrauterine air breathing is an order of magnitude, from a range of 10-12 to 110-120 Torr. The contributions of oxygen and the volume and pressure relationships of ventilatory support to lung injury are not easily distinguished in the clinical setting. Sequential changes in inspired air or 100% oxygen were studied in 536 newborn rabbits without ventilatory support. Bilateral cervical vagotomies (BCV) were performed at 24 hours post natal to induce ventilatory distress which eventuates in hyaline membrane disease. The sequences applied yielded evidence for an induced state of oxygen dependency from oxygen use which was reflected in differences in survival and the extent of pulmonary injury. The median survival for animals kept in air throughout was 3 hours. Oxygen before vagotomy or during the first 3 hours afterwards extended the survival significantly but produced more extensive, more severe, and more rapid lung lesions. Returning animals to air after prior oxygen exposure reduced the number of survivors past 10 hours and shortened the maximum survival in those groups. These features indicate the development of a dependency of the defense mechanisms on the availability of oxygen at the higher level for metabolic and possibly other aspects of the pulmonary and systemic response to injury, beyond the usual physiological need.Subset analysis revealed additive and latent effects of oxygen and demonstrated a remarkable rapidity in onset of severe lesions under some circumstances, illustrating the toxicity of oxygen per se.

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Role of the Nrf2/HO-1 axis in bronchopulmonary dysplasia and hyperoxic lung injuries

et al. 2017

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Bronchopulmonary dysplasia (BPD) is a chronic illness that usually originates in preterm newborns. Generally, BPD is a consequence of respiratory distress syndrome (RDS) which, in turn, comes from the early arrest of lung development and the lack of pulmonary surfactant. The need of oxygen therapy to overcome premature newborns' compromised respiratory function generates an increasing amount of reactive oxygen species (ROS), the onset of sustained oxidative stress (OS) status, and inflammation in the pulmonary alveoli deputies to respiratory exchanges. BPD is a severe and potentially life-threatening disorder that in the most serious cases, can open the way to neurodevelopmental delay. More importantly, there is no adequate intervention to hamper or treat BPD. This perspective article seeks to review the most recent and relevant literature describing the very early stages of BPD and hyperoxic lung injuries focussing on nuclear factor erythroid derived 2 (Nrf2)/heme oxygenase-1 (HO-1) axis. Indeed, Nrf2/HO1 activation in response to OS induced lung injury in preterm concurs to the induction of certain number of antioxidant, anti-inflammatory, and detoxification pathways that seem to be more powerful than the activation of one single antioxidant gene. These elicited protective effects are able to counteract/mitigate all multifaceted aspects of the disease and may support novel approaches for the management of BPD.

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On the Pulmonary Toxicity of Oxygen I. The Relationship of Oxygen Content to the Effect of Oxygen on the Lung

Cited by 8 publications

References 0 publications

On the pulmonary toxicity of oxygen. 4. The thyroid arena

On the pulmonary toxicity of oxygen. 4. The thyroid arena

On the pulmonary toxicity of oxygen: III. The induction of oxygen dependency by oxygen use

Role of the Nrf2/HO-1 axis in bronchopulmonary dysplasia and hyperoxic lung injuries

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