Changes in respiratory control in humans induced by 8 h of hyperoxia.
In humans, 8 h of isocapnic hypoxia causes a progressive rise in ventilation associated with increases in the acute ventilatory responses to hypoxia (AHVR) and hypercapnia (AHCVR). To determine whether 8 h of hyperoxia causes the converse of these effects, three 8-h protocols were compared in 14 subjects: 1) poikilocapnic hyperoxia, with end-tidal PO(2) (PET(O(2))) = 300 Torr and end-tidal PCO(2) (PET(CO(2))) uncontrolled; 2) isocapnic hyperoxia, with PET(O(2)) = 300 Torr and PET(CO(2)) maintained at the subject's normal air-breathing level; and 3) control. Ventilation was measured hourly. AHVR and AHCVR were determined before and 0.5 h after each exposure. During isocapnic hyperoxia, after an initial increase, ventilation progressively declined (P < 0.01, ANOVA). After exposure to hyperoxia, 1) AHVR declined (P < 0.05); 2) ventilation at fixed PET(CO(2)) decreased (P < 0.05); and 3) air-breathing PET(CO(2)) increased (P < 0.05); but 4) no significant changes in AHCVR or intercept were demonstrated. In conclusion, 8 h of hyperoxia have some effects opposite to those found with 8 h of hypoxia, indicating that there may be some "acclimatization to hypoxia" at normal sea-level values of PO(2).
University Laboratory of Physiology, University of Oxford, United Kingdom.
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Ren
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Fatemian
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Robbins
D000293:Adolescent; D000328:Adult; D000465:Algorithms; D001784:Blood Gas Analysis; D002245:Carbon Dioxide / Q000097:blood; D002628:Chemoreceptor Cells / Q000502:physiology; D005260:Female; D006801:Humans; D006863:Hydrogen-Ion Concentration; D018496:Hyperoxia / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D008954:Models, Biological; D010100:Oxygen / Q000633:toxicity; D015656:Respiratory Mechanics / Q000502:physiology*
D002245:Carbon Dioxide; D010100:Oxygen