Maximun flow-volume, static pressure-volume, and maximum flow static recoil curves of three groups of nonsmoking, normal subjects (young men, young women, elderly women) were used to assess age and sex differences in pulmonary mechanics. No significant sex differences in maximum flow were seen but the young men showed higher lung recoil pressures at full inflation. When the influence of the inspiratory muscles and chest wall was excluded by exponential extrapolation of the pressure-volume curves to a maximum volume the bulk elastic properties of the lungs of young men and women appeared identical. Loss of maximum expiratory flow at low lung volumes and of lung recoil pressure occurred with age in nonsmoking women in whom emphysema should be minimal and therefore indicate true physiological effects of aging. The changes in pulmonary mechanics with age are consistent with an increase in unstressed dimensions and loss of elastic recoil of both alveoli and airways.
To investigate the effect of alae nasi (AN) activation on nasal resistance, we monitored AN electromyographic (EMG) activity in 17 healthy subjects using surface electrodes placed on either side of the external nares and measured inspiratory nasal resistance utilizing the method of posterior rhinometry. With CO2 inhalation (6 subj), AN EMG activity increased as nasal resistance fell 23 +/- 5% (P less than 0.01). In the same subjects, voluntary flaring of the external nares also increased AN EMG and decreased nasal resistance by 29 +/- 5% (P less than 0.01). Nasal resistance was altered by nasal flaring and CO2 inhalation even after administration of a topical nasal vasoconstrictive spray (8 subj). In six subjects, voluntary nasal flaring or inhibition with the mouth closed produced a 21 +/- 12% change (P less than 0.01) in total airway resistance as measured by body plethysmography. We conclude that activation of the alae nasi will decrease nasal and total airway resistance during voluntary nasal flaring and during CO2 inhalation and thus should be considered in any studies of upper airway resistance.
The increased minute ventilation (VE) associated with exercise produces similar degrees of airway cooling in normal and asthmatic subjects, but only those with asthma develop postexertional bronchoconstriction in response to this stimulus. We have found that when normal subjects breathing subfreezing air perform isocapnic hyperventilation to levels exceeding those associated with even exhausting exercise, 1-s forced expiratory volumes and maximum midexpiratory flow rates fall significantly. When tests more sensitive in detecting bronchoconstriction are employed, changes are seen at lower levels of hyperventilation that simulate the VE associated with moderately heavy work loads. We conclude that normal subjects respond to airway cooling, but are much less sensitive than those with asthma.
Bronchodilatation was produced in normal subjects by the inhalation of a parasympatholytic agent (atropine) and the response was compared to that occurring after the inhalation of a beta-adrenergic agent (isoetharine). Doses were chosen that resulted in equivalent increases in specific airway conductance (78 +/- 9% for atropine; 88 +/- 21% for isoetharine). Anatomic dead space and volume at the onset of the terminal nitrogen rise (closing volume) were measured before and after each agent. Although there was no difference in the degree of overall bronchodilatation after the two drugs, anatomical dead space increased significantly more after atropine than isoetharine (+17% vs. +6%, P less than 0.01), and closing volume increased significantly after isoetharine (P less than 0.005) but did not change with atropine. We interpret these differences to indicate a greater effect of cholinergic antagonists on the more central airways and a greater effect of beta-adrenergic stimulants on peripheral airways.
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