Journal of applied physiology
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Children snore less than adults and have fewer obstructive apneas, suggesting a less collapsible upper airway. We therefore hypothesized that the compensatory upper airway responses to subatmospheric pressure loading decrease with age because of changes in upper airway structure and ventilatory drive. We measured upper airway upstream pressure-flow relationships during sleep in 20 nonsnoring, nonobese children and adults. ⋯ We conclude that the upper airway compensatory responses to subatmospheric pressure loading decrease with age. This is associated with increased body mass index, even in nonsnoring, nonobese subjects. Ventilatory drive during sleep plays a role in modulating upper airway responses.
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This study was designed to determine the responses of lung volume and respiratory resistance (Rrs) to decreasing levels of continuous negative airway pressure (CNAP). Twenty normal subjects were studied in the basal state and under CNAP levels of -5, -10, and -15 hPa. Rrs was measured by the forced oscillation technique (4-32 Hz). ⋯ At the lowest CNAP level, R(0) and R(16) reached 198 +/- 13 and 175 +/- 9% of their respective basal values. The CNAP-induced increase in R(0) was significantly higher than that in R(16) (P < 0.004). Our results demonstrate that the CNAP-induced increase in Rrs does not result from a direct lung volume effect only and strongly suggest the involvement of other factors affecting both intrathoracic and extrathoracic airway caliber.
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Adequate assessment of circulatory and gas-exchange interactions may involve the quantification of the Haldane effect (HE) and of the changes in blood PCO(2) mediated by changes in Hb-O(2) saturation and O(2)-linked CO(2) binding. This is commonly prevented by the complexity of the involved calculations. ⋯ This formula is useful in assessing the impact of HE on Pv(CO(2)) and venoarterial PCO(2) gradient and the survival advantage offered by HE in extreme conditions. Use may be extended to all investigative and clinical settings in which changes in blood O(2) saturation and O(2)-linked CO(2) binding must be converted into the corresponding changes in dissolved CO(2) and PCO(2).