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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Pulmonary function in men after oxygen breathing at 3.0 ATA for 3.5 h. 175 24

Animal studies suggest that pulmonary oxygen toxicity proceeds more slowly in diluted oxygen breathing mixtures than in pure oxygen at the same inspired partial pressure. We exposed 12 healthy subjects to air at 5 ATA (PiO2 = 1.05 ATA) in a hyperbaric chamber for 48 h, and compared the rate of development of symptoms of O2 toxicity to rates seen in previous studies using 100% O2 at 1 ATA. Symptoms consisted of chest tightness, cough, substernal discomfort, exertional dyspnea, anorexia, nausea and vomiting, headache and digital paresthesias starting at about 12 h, and continuing several days into the recovery period. Pulmonary function changes consisted of significant decrements in vital capacity, flow rates, and DLCO. Initial recovery was in a 0.50 ATA oxygen atmosphere, with the majority of subjects showing definite recovery in both symptoms and pulmonary function. Subjects showed complete recovery in about 8 d, although symptoms of fatigue and exertional dyspnea continued for a month in some cases. In contrast, none of the above changes were noted in an additional 6 subjects exposed to a 5 ATA environment with 6% oxygen (PiO2 = 0.30 ATA). No change in resting gas exchange, as indicated by alveolar-arterial oxygen gradients, was detected in either group. Comparison of these data to that for pure oxygen studies reveals no significant difference in the progression or character of pulmonary oxygen toxicity.
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PMID:Progression of and recovery from pulmonary oxygen toxicity in humans exposed to 5 ATA air. 361 41