Pulmonary function in men after oxygen breathing at 3.0 ATA for 3.5 h

J. M. Clark, Robert Jackson, C. J. Lambertsen, R. Gelfand, W. D B Hiller, M. Unger

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

As a pulmonary component of Predictive Studies V, designed to determine O2 tolerance of multiple organs and systems in humans at 3.0-1.5 ATA, pulmonary function was evaluated at 1.0 ATA in 13 healthy men before and after O2 exposure at 3.0 ATA for 3.5 h. Measurements included flow-volume loops, spirometry, and airway resistance (Raw) (n = 12); CO diffusing capacity (n = 11); closing volumes (n = 6); and air vs. HeO2 forced vital capacity maneuvers (n = 5). Chest discomfort, cough, and dyspnea were experienced during exposure in mild degree by most subjects. Mean forced expiratory volume in 1 s (FEV1) and forced expiratory flow at 25-75% of vital capacity (FEF25-75) were significantly reduced postexposure by 5.9 and 11.8%, respectively, whereas forced vital capacity was not significantly changed. The average difference in maximum midexpiratory flow rates at 50% vital capacity on air and HeO2 was significantly reduced postexposure by 18%. Raw and CO diffusing capacity were not changed postexposure. The relatively large change in FEF25-75 compared with FEV1, the reduction in density dependence of flow, and the normal Raw postexposure are all consistent with flow limitation in peripheral airways as a major cause of the observed reduction in expiratory flow. Postexposure pulmonary function changes in one subject who convulsed at 3.0 h of exposure are compared with corresponding average changes in 12 subjects who did not convulse.

Original languageEnglish
Pages (from-to)878-885
Number of pages8
JournalJournal of Applied Physiology
Volume71
Issue number3
StatePublished - Jan 1 1991
Externally publishedYes

Fingerprint

Vital Capacity
Respiration
Oxygen
Lung
Forced Expiratory Volume
Carbon Monoxide
Closing Volume
Air
Airway Resistance
Spirometry
Cough
Dyspnea
Thorax

Keywords

  • hyperbaric oxygen
  • oxygen limits
  • oxygen poisoning
  • oxygen tolerance in humans
  • pulmonary oxygen toxicity

ASJC Scopus subject areas

  • Endocrinology
  • Physiology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Clark, J. M., Jackson, R., Lambertsen, C. J., Gelfand, R., Hiller, W. D. B., & Unger, M. (1991). Pulmonary function in men after oxygen breathing at 3.0 ATA for 3.5 h. Journal of Applied Physiology, 71(3), 878-885.

Pulmonary function in men after oxygen breathing at 3.0 ATA for 3.5 h. / Clark, J. M.; Jackson, Robert; Lambertsen, C. J.; Gelfand, R.; Hiller, W. D B; Unger, M.

In: Journal of Applied Physiology, Vol. 71, No. 3, 01.01.1991, p. 878-885.

Research output: Contribution to journalArticle

Clark, JM, Jackson, R, Lambertsen, CJ, Gelfand, R, Hiller, WDB & Unger, M 1991, 'Pulmonary function in men after oxygen breathing at 3.0 ATA for 3.5 h', Journal of Applied Physiology, vol. 71, no. 3, pp. 878-885.
Clark JM, Jackson R, Lambertsen CJ, Gelfand R, Hiller WDB, Unger M. Pulmonary function in men after oxygen breathing at 3.0 ATA for 3.5 h. Journal of Applied Physiology. 1991 Jan 1;71(3):878-885.
Clark, J. M. ; Jackson, Robert ; Lambertsen, C. J. ; Gelfand, R. ; Hiller, W. D B ; Unger, M. / Pulmonary function in men after oxygen breathing at 3.0 ATA for 3.5 h. In: Journal of Applied Physiology. 1991 ; Vol. 71, No. 3. pp. 878-885.
@article{73cb4a9769ff45bf8b8bd9d7eed6aba4,
title = "Pulmonary function in men after oxygen breathing at 3.0 ATA for 3.5 h",
abstract = "As a pulmonary component of Predictive Studies V, designed to determine O2 tolerance of multiple organs and systems in humans at 3.0-1.5 ATA, pulmonary function was evaluated at 1.0 ATA in 13 healthy men before and after O2 exposure at 3.0 ATA for 3.5 h. Measurements included flow-volume loops, spirometry, and airway resistance (Raw) (n = 12); CO diffusing capacity (n = 11); closing volumes (n = 6); and air vs. HeO2 forced vital capacity maneuvers (n = 5). Chest discomfort, cough, and dyspnea were experienced during exposure in mild degree by most subjects. Mean forced expiratory volume in 1 s (FEV1) and forced expiratory flow at 25-75{\%} of vital capacity (FEF25-75) were significantly reduced postexposure by 5.9 and 11.8{\%}, respectively, whereas forced vital capacity was not significantly changed. The average difference in maximum midexpiratory flow rates at 50{\%} vital capacity on air and HeO2 was significantly reduced postexposure by 18{\%}. Raw and CO diffusing capacity were not changed postexposure. The relatively large change in FEF25-75 compared with FEV1, the reduction in density dependence of flow, and the normal Raw postexposure are all consistent with flow limitation in peripheral airways as a major cause of the observed reduction in expiratory flow. Postexposure pulmonary function changes in one subject who convulsed at 3.0 h of exposure are compared with corresponding average changes in 12 subjects who did not convulse.",
keywords = "hyperbaric oxygen, oxygen limits, oxygen poisoning, oxygen tolerance in humans, pulmonary oxygen toxicity",
author = "Clark, {J. M.} and Robert Jackson and Lambertsen, {C. J.} and R. Gelfand and Hiller, {W. D B} and M. Unger",
year = "1991",
month = "1",
day = "1",
language = "English",
volume = "71",
pages = "878--885",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "3",

}

TY - JOUR

T1 - Pulmonary function in men after oxygen breathing at 3.0 ATA for 3.5 h

AU - Clark, J. M.

AU - Jackson, Robert

AU - Lambertsen, C. J.

AU - Gelfand, R.

AU - Hiller, W. D B

AU - Unger, M.

PY - 1991/1/1

Y1 - 1991/1/1

N2 - As a pulmonary component of Predictive Studies V, designed to determine O2 tolerance of multiple organs and systems in humans at 3.0-1.5 ATA, pulmonary function was evaluated at 1.0 ATA in 13 healthy men before and after O2 exposure at 3.0 ATA for 3.5 h. Measurements included flow-volume loops, spirometry, and airway resistance (Raw) (n = 12); CO diffusing capacity (n = 11); closing volumes (n = 6); and air vs. HeO2 forced vital capacity maneuvers (n = 5). Chest discomfort, cough, and dyspnea were experienced during exposure in mild degree by most subjects. Mean forced expiratory volume in 1 s (FEV1) and forced expiratory flow at 25-75% of vital capacity (FEF25-75) were significantly reduced postexposure by 5.9 and 11.8%, respectively, whereas forced vital capacity was not significantly changed. The average difference in maximum midexpiratory flow rates at 50% vital capacity on air and HeO2 was significantly reduced postexposure by 18%. Raw and CO diffusing capacity were not changed postexposure. The relatively large change in FEF25-75 compared with FEV1, the reduction in density dependence of flow, and the normal Raw postexposure are all consistent with flow limitation in peripheral airways as a major cause of the observed reduction in expiratory flow. Postexposure pulmonary function changes in one subject who convulsed at 3.0 h of exposure are compared with corresponding average changes in 12 subjects who did not convulse.

AB - As a pulmonary component of Predictive Studies V, designed to determine O2 tolerance of multiple organs and systems in humans at 3.0-1.5 ATA, pulmonary function was evaluated at 1.0 ATA in 13 healthy men before and after O2 exposure at 3.0 ATA for 3.5 h. Measurements included flow-volume loops, spirometry, and airway resistance (Raw) (n = 12); CO diffusing capacity (n = 11); closing volumes (n = 6); and air vs. HeO2 forced vital capacity maneuvers (n = 5). Chest discomfort, cough, and dyspnea were experienced during exposure in mild degree by most subjects. Mean forced expiratory volume in 1 s (FEV1) and forced expiratory flow at 25-75% of vital capacity (FEF25-75) were significantly reduced postexposure by 5.9 and 11.8%, respectively, whereas forced vital capacity was not significantly changed. The average difference in maximum midexpiratory flow rates at 50% vital capacity on air and HeO2 was significantly reduced postexposure by 18%. Raw and CO diffusing capacity were not changed postexposure. The relatively large change in FEF25-75 compared with FEV1, the reduction in density dependence of flow, and the normal Raw postexposure are all consistent with flow limitation in peripheral airways as a major cause of the observed reduction in expiratory flow. Postexposure pulmonary function changes in one subject who convulsed at 3.0 h of exposure are compared with corresponding average changes in 12 subjects who did not convulse.

KW - hyperbaric oxygen

KW - oxygen limits

KW - oxygen poisoning

KW - oxygen tolerance in humans

KW - pulmonary oxygen toxicity

UR - http://www.scopus.com/inward/record.url?scp=0025833203&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025833203&partnerID=8YFLogxK

M3 - Article

C2 - 1757324

AN - SCOPUS:0025833203

VL - 71

SP - 878

EP - 885

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 3

ER -