Aviation, space, and environmental medicine · 2006
Ventilatory effects of prolonged hyperoxia at pressures of 1.5-3.0 ATA.
Клиническое исследованиеСтатьяПоддержка исследования: вне правительства СШАПоддержка правительства СШАНазвание и аннотация: Перевод в очереди
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Gelfand Robert, Lambertsen Christian J, Clark James M
Аннотация
INTRODUCTION: It was hypothesized that long-duration exposures to toxic levels of hyperoxia would have effects on respiratory control function or activity.
METHODS: Ventilatory parameters of human subjects breathing spontaneously at rest were measured before, during, and after hyperoxia in a study of organ systems' tolerance to toxic O2 exposures at 1.5 ATA (17.7 h), 2.0 ATA (9.3 h), 2.5 ATA (5.7 h) and 3.0 ATA (3.5 h).
RESULTS: Average neurotoxic changes in ventilatory parameters during and after prolonged hyperoxia were mild. They included: 1) timing component of ventilation decreased progressively with exposure duration at all four O2 pressures, slopes increased with O2 pressure, changes were significantly late in exposure at 1.5 ATA (-11%) and 3.0 ATA (-10%); 2) post-O2 exposure respiratory rates were significantly above controls by 15% to 59%; and 3) ventilation increased significantly by 20% late during the 1.5 ATA O2 exposures. There were severe neurotoxic changes prior to occurrence of an "O2 convulsion" at 3.0 ATA in one subject. Expiratory time increased by 184%; resultant reductions in respiratory rate and ventilation caused respiratory Pco2 increase, accelerating rate of brain O2 poisoning. Significant nontoxic physiological hyperventilation (21% to 45% above control) early in hyperoxia at all exposure pressures persisted throughout hyperoxia, and reversed post-O2 exposure. Hyperventilation increased and end-tidal Pco2 decreased as inspired PO2 increased. Changes reached maximum values at approximately 2.0 ATA.
DISCUSSION: Hyperoxia has concurrent toxic and physiological effects on respiratory control; degrees depend on O2 dose (exposure pressure and duration).
METHODS: Ventilatory parameters of human subjects breathing spontaneously at rest were measured before, during, and after hyperoxia in a study of organ systems' tolerance to toxic O2 exposures at 1.5 ATA (17.7 h), 2.0 ATA (9.3 h), 2.5 ATA (5.7 h) and 3.0 ATA (3.5 h).
RESULTS: Average neurotoxic changes in ventilatory parameters during and after prolonged hyperoxia were mild. They included: 1) timing component of ventilation decreased progressively with exposure duration at all four O2 pressures, slopes increased with O2 pressure, changes were significantly late in exposure at 1.5 ATA (-11%) and 3.0 ATA (-10%); 2) post-O2 exposure respiratory rates were significantly above controls by 15% to 59%; and 3) ventilation increased significantly by 20% late during the 1.5 ATA O2 exposures. There were severe neurotoxic changes prior to occurrence of an "O2 convulsion" at 3.0 ATA in one subject. Expiratory time increased by 184%; resultant reductions in respiratory rate and ventilation caused respiratory Pco2 increase, accelerating rate of brain O2 poisoning. Significant nontoxic physiological hyperventilation (21% to 45% above control) early in hyperoxia at all exposure pressures persisted throughout hyperoxia, and reversed post-O2 exposure. Hyperventilation increased and end-tidal Pco2 decreased as inspired PO2 increased. Changes reached maximum values at approximately 2.0 ATA.
DISCUSSION: Hyperoxia has concurrent toxic and physiological effects on respiratory control; degrees depend on O2 dose (exposure pressure and duration).