Effect of posture on upper and lower rib cage motion and tidal volume during diaphragm pacing.

We monitored changes in upper and lower rib cage dimensions and tidal volume during bilateral phrenic nerve pacing in a quadraplegic subject with a flaccid chest wall paralysis. Both upper and lower rib cage showed inward (paradoxical) motion during paced breaths in supine (horizontal) and upright positions on a tilt table. In both postures, abdominal compression changed only the lower rib cage to orthodox motion. Abdominal compression in the supine posture decreased tidal volume 10 to 20%, while end-inspiratory diaphragm length, assessed from end-expiratory volume, did not change. Abdominal compression in the upright posture caused end-expiratory volume to fall and increased tidal volume 200%. These observations suggest that isolated diaphragm contraction can move the lower ribs independently from the upper ribs and that tidal volume is determined both by the resting length of the diaphragm and by diaphragmatic load.

Experimental induction of chronic bronchitis in dogs: effects on airway obstruction and responsiveness.

Chronic bronchitis was induced in 6 mongrel dogs by chronic exposure to SO2 gas; the degree of chronic airway obstruction and the effects on airway responsiveness to inhaled histamine, carbachol, and prostaglandin F2 alpha were examined. Five dogs developed chronic airway obstruction, as indicated by an increase in pulmonary resistance, and clinical mucous hypersecretion. In addition, in each of the animals in which chronic airway obstruction developed there was a decrease in the airway responsiveness to inhaled mediators. Those findings demonstrate that induction of chronic bronchitis in dogs results in hyporesponsiveness to inhaled mediators, a finding distinctly different from that reported in human subjects with naturally occurring disease.

Alae nasi activation and nasal resistance in healthy subjects.

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.

Alveolar pressure-airflow characteristics in humans breathing air, He-O2, and SF6-O2.

In a system of rigid tubes under steady flow conditions, the coefficient of friction [CF = 2 delta P/(rho V2/A2)] (where delta P is pressure drop, rho is density, V is flow, and A is cross-sectional area) should be a unique function of Reynolds' number (Re). Recently it has been shown that at any given Re, the value of CF using transpulmonary pressure (PL) was lower when breathing He-O2 compared with air (Lisboa et al., J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 48: 878-885, 1980). One explanation for this discontinuity is that PL includes the pressure drop due to tissue viscance, which is independent of V, and thus would lead to an overestimate of CF on air compared with He-O2 at any Re. We tested this hypothesis by measuring V related to alveolar pressure, rather than PL, in normal subjects breathing air, He-O2, and SF6-O2. In each subject, for a given Re, CF was greatest breathing SF6-O2 and lowest breathing He-O2, similar to results using PL. Thus tissue viscance is not the sole cause of the discontinuous plot of CF vs. Re, and this phenomenon must be due to other factors, such as changing geometry or nonsteady behavior.

Inhalation patterns and predominant site of bronchoconstriction in healthy subjects.

To determine the relationship between changes in density dependence of maximal expiratory flow and changes in the predominant site of bronchoconstriction, we altered the pattern of inhalation of a methacholine aerosol to achieve deposition either centrally (by short choppy breaths) or peripherally (by slow deep breaths). Partial expiratory flow volume curves on air and on 80% helium-20% oxygen (HeO2) were recorded in six healthy subjects before and after each pattern of methacholine inhalation. We varied concentrations of methacholine and number of inhalations to achieve equivalent degrees of bronchoconstriction as assessed by decreases in maximal flow (Vmax) on air, which fell 27% from control values. Vmax on HeO2 also fell after both inhalation patterns. Density dependence (Vmax on HeO2 divided by Vmax on air) decreased following slow deep breaths of bronchoconstrictor aerosol, and increased following short choppy breaths. In three subjects, inhalation of radiolabeled methacholine aerosol confirmed that the slow deep pattern was associated with a diffuse, more peripheral deposition, whereas the short choppy pattern led to central deposition. We conclude that changes in density dependence reflect the predominant site of obstruction after acute methacholine aerosol challenge in healthy subjects.

Airway effects of respiratory heat loss in normal subjects.

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.

Pattern and mechanism of airway response to hypocapnia in normal subjects.

We examined the bronchoconstriction produced by airway hypocapnia in normal subjects. Maximal expiratory flow at 25% vital capacity on partial expiratory flow-volume (PEFV) curves fell during hypocapnia both on air and on an 80% helium- 20% oxygen mixture. Density dependence also fell, suggesting predominantly small airway constriction. The changes seen on PEFV curves were not found on maximal expiratory flow-volume curves, indicating the inhalation to total lung capacity substantially reversed the constriction. Pretreatment with a beta-sympathomimetic agent blocked the response, whereas atropine pretreatment did not, suggesting that hypocapnia affects airway smooth muscle directly, not via cholinergic efferents.

Distribution of bronchodilatation in normal subjects: beta agonist versus atropine.

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.