Extension of pulmonary O2 tolerance in man at 2 ATA by intermittent O2 exposure

Hendricks, P. L.; Hall, David A.; Hunter, William L.; Haley, Patrick J.

doi:10.1152/jappl.1977.42.4.593

Cited by 46 publications

(24 citation statements)

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“…Pulmonary oxygen toxicity is attenuated when oxygen is administered intermittently, but that is within a range of oxygen pressures of 42-200 kPa, which is much higher than in this study (Hendricks et al 1977). In an analysis of experimental deep dives in the depth range of 110-450 m including 118 dives where P O 2 was constant at 50-60 kPa during decompression, there was a relationship between the reduction in Tl CO and cumulative hyperoxic exposure (Thorsen et al 1994).…”

Section: Discussioncontrasting

confidence: 48%

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No changes in lung function after a saturation dive to 2.5 MPa with intermittent reduction in $$ P_{{{{\rm O}}_{{{\rm 2}}} }} $$ during decompression

et al. 2006

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Decompression stress and exposure to hyperoxia may cause a reduction in transfer factor of the lung for carbon monoxide and in maximal aerobic capacity after deep saturation dives. In this study lung function and exercise capacity were assessed before and after a helium-oxygen saturation dive to a pressure of 2.5 MPa where the decompression rate was reduced compared with previous deep dives, and the hyperoxic exposure was reduced by administering oxygen intermittently at pressures of 50 and 30 kPa during decompression. Eight experienced divers of median age 41 years (range 29-48) participated in the dive. The incidence of venous gas microemboli was low compared with previous deep dives. Except for one subject having treatment for decompression sickness, no changes in lung function or angiotensin converting enzyme, a marker of pulmonary endothelial cell damage, were demonstrated. The modified diving procedures with respect to decompression rate and hyperoxic exposure may have contributed to the lack of changes in lung function in this dive compared with previous deep saturation dives.

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Section: Discussioncontrasting

confidence: 48%

“…Pulmonary oxygen toxicity is attenuated when exposure is intermittent (Hendricks et al 1977). VGM may cause direct mechanical injury to the vascular surface layer and endothelial cells with shedding of the endothelial layer in arterioles (Nossum et al 1999), and mechanical obstruction of pulmonary blood flow.…”

Section: Introductionmentioning

confidence: 99%

No changes in lung function after a saturation dive to 2.5 MPa with intermittent reduction in $$ P_{{{{\rm O}}_{{{\rm 2}}} }} $$ during decompression

et al. 2006

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“…Inadvertent exposure of patients with normal lungs to prolonged hyperoxia resulted in clinical findings compatible with oxygen toxicity (12). Exposure of normal humans to oxygen at elevated pressure (that is, greater than 1 ATA O 2 ) has indicated a shorter duration of exposure for equivalent pulmonary symptoms and function changes (8,10,16,18). Pulmonary-related death has been reported for one patient in the normobaric O 2 exposure group (12) and another with hyperbaric exposure (9).…”

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confidence: 99%

Hyperoxia and acute lung injury

Fisher¹,

Beers²

2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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TO THE EDITOR: The review by has misleading and potentially dangerous statements concerning the role of hyperoxia in human acute lung injury (ALI). Table 4 states "in normal human lungs, 100% oxygen has not induced lung injury . . . " The text states that most mammalian species develop respiratory distress and die with exposure to 100% oxygen, but the "same findings have not been reproduced in humans with normal lungs . . . " That statement is essentially true (fortunately) but mainly because very few studies of potentially lethal hyperoxia have been carried out in individuals with normal lungs, for obvious reasons. The one study referenced in the review (1) was carried out in patients with irreversible brain injury, which may have influenced the pulmonary response to hyperoxia, and indeed a subsequent similar study demonstrated significant lung injury (13). Studies of normal individuals exposed experimentally to 100% oxygen at normal pressure (i.e., 1 ATA) have shown evidence of tracheobronchitis and changes in vital capacity, diffusing capacity, and lung permeability (2-5, 7, 17). Inadvertent exposure of patients with normal lungs to prolonged hyperoxia resulted in clinical findings compatible with oxygen toxicity (12). Exposure of normal humans to oxygen at elevated pressure (that is, greater than 1 ATA O 2 ) has indicated a shorter duration of exposure for equivalent pulmonary symptoms and function changes (8,10,16,18). Pulmonary-related death has been reported for one patient in the normobaric O 2 exposure group (12) and another with hyperbaric exposure (9). Thus evidence of lung abnormalities with severity proportional to the partial pressure of oxygen has been demonstrated in normal human lungs similar to the findings with experimental animals. It is known that different species, and indeed strains of the same species as well as individuals from the same strain, show varying sensitivity to the toxic effects of oxygen (11). Rats exposed to 0.8 ATA O 2 become tolerant to 1 ATA O 2 but uniformly die when subsequently exposed to higher (1.5 ATA) O 2 partial pressures (14), emphasizing the importance of O 2 "dose." Parenthetically, the dose range for lethality (approximately 0.8 -1.5 ATA) is quite narrow compared with many toxicants where dose sensitivity of various species may vary by more than an order of magnitude. So the important question is, what is the dose range for human pulmonary oxygen toxicity? Based on the limited number of human studies but with analogy to nonhuman primates (6), the "average" human might require O 2 at 1.1 or 1.2 ATA to reach a lethal concentration. If that is the case, a large segment of the human population might be spared ALI and lethality with 100% oxygen at 1 ATA. However, that concentration of oxygen could prove to be lethal for that fraction of the population whose resistance to oxidant stress is less than the population mean. All indications are that hyperoxia in animals (with appropriate consideration of dose) does serve as a model for human ALI associated with oxidant...

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“…There is a dose-dependent reduction in vital capacity with continuous exposure to a PO 2 >50 kPa, as characterized by CLARK and LAMBERTSEN [2]. It has also been shown that this effect is attenuated by intermittent exposure to up to the same cumulative dose of oxygen [3] and tolerance to the oxidative stress develops. HBO treatment protocols and diving procedures are based on these doseresponse relationships and practical experience.…”

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confidence: 99%

Effects of a standard hyperbaric oxygen treatment protocol on pulmonary function

Thorsen¹,

Aanderud²,

Aasen³

1998

Eur Respir J

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Recompression and hyperbaric oxygen (HBO) are used in the treatment for diving-related diseases such as decompression sickness and arterial gas embolism. For a long time HBO has also been shown to be effective in carbon monoxide poisoning and anaerobic infections. More recently, HBO has been shown to have supplementary effects in the treatment of other disorders characterized by local ischaemia. An increase in local oxygen supply due to an increased gradient for diffusion is achieved by increasing the partial pressure of oxygen (PO 2 ) in inspired gas. This results in local stimulation of fibroblast proliferation and collagen synthesis, angiogenesis and enhanced granulocyte function and peroxidase activity in ischaemic tissue. In this way, HBO treatment is an effective adjunct in the treatment of osteoradionecrosis, chronic osteomyelitis, diabetic leg ulcers and radiation-induced proctitis and cystitis. On an experimental basis, HBO treatment is currently evaluated as a supplement in the treatment of several other disorders. Indications for HBO treatment have been worked out by the Undersea and Hyperbaric Society [1], differentiating between indications where HBO has been shown to have a definite effect based on controlled clinical studies and indications where HBO still has to be considered experimental. In this setting, HBO treatment is usually given for 90 min daily at a PO 2 of 200-280 kPa for 20-30 days.Toxic pulmonary effects of exposure to hyperoxia are well known. There is a dose-dependent reduction in vital capacity with continuous exposure to a PO 2 >50 kPa, as characterized by CLARK and LAMBERTSEN [2]. It has also been shown that this effect is attenuated by intermittent exposure to up to the same cumulative dose of oxygen [3] and tolerance to the oxidative stress develops. HBO treatment protocols and diving procedures are based on these doseresponse relationships and practical experience. Ser-ious pulmonary oxygen toxicity has not been reported with this form of HBO treatment. However, systematic studies to quantify the effect on pulmonary function of commonly used HBO treatment protocols are lacking. Methods PatientsTwenty consecutive patients (10 male) undergoing treatment for ischaemic leg or foot ulcers, chronic osteomyelitis, delayed healing of fractures with pseudarthrosis or pelvic radionecrosis were included in the study. Patients with lung disease, former irradiation of the head, neck or thorax as part of the treatment for the primary disease, current smokers and patients with radiologically abnormal A reduction in small airways conductance is consistent with other studies where total oxygen exposures have been below the limit causing toxic pulmonary effects traditionally measured as a reduction in vital capacity. This effect is not considered to be of any clinical significance for patients treated with hyperbaric oxygen unless repeated treatment series are to be given.

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Extension of pulmonary O2 tolerance in man at 2 ATA by intermittent O2 exposure

Cited by 46 publications

References 0 publications

No changes in lung function after a saturation dive to 2.5 MPa with intermittent reduction in $$ P_{{{{\rm O}}_{{{\rm 2}}} }} $$ during decompression

No changes in lung function after a saturation dive to 2.5 MPa with intermittent reduction in $$ P_{{{{\rm O}}_{{{\rm 2}}} }} $$ during decompression

Hyperoxia and acute lung injury

Effects of a standard hyperbaric oxygen treatment protocol on pulmonary function

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