Head position modifies upper airway resistance in men

We measured in healthy volunteers airway resistance (R(aw)), resistance of the respiratory system (Rrs), and supralaryngeal resistance (Rsl) in the following head positions: neutral, extended, and partially and fully flexed. Sagittal magnetic resonance images of the upper airways were recorded in neutral and flexed head positions. We observed significant increases in Raw (P less than 0.01), Rrs (P less than 0.001), and Rsl (P less than 0.001) in the flexed position, with respect to the neutral one, and corresponding decreases of specific airway and specific respiratory conductances. Resistances decreased (although not significantly) when the subjects' heads were extended. A decrease in both diameter and surface area of the hypopharyngeal airways (as shown by magnetic resonance images) with total head flexion was accompanied by significant increases in all measured resistances. Changes in the caliber of hypopharynx appear to be responsible for the increase in resistance during head flexion.     

Ventilatory and diaphragmatic EMG changes during negative-pressure ventilation in healthy subjects

To evaluate the response of normal subjects to assisted ventilation, we studied 6 naive healthy subjects before and during negative-pressure ventilation (NPV) with "low" (-10 cmH2O) and "high" (-30 cmH2O) pressures in an Emerson tank respirator. Ventilation was measured with an inductive plethysmograph (Respitrace), and diaphragmatic electromyogram (DEMG) was studied with a bipolar esophageal electrode. During NPV a 1:1 phase lock was observed between subjects and iron lung frequency in all subjects. Tidal volume increased in most subjects, more with high than with low pressures (P less than 0.05), whereas DEMG increased, decreased, or showed no change. Postinspiratory inspiratory diaphragmatic activity (PIIA) significantly increased during high-pressure NPV and was accompanied by an increase in tonic DEMG in one-half of the subjects. Voluntary relaxation resulted in a decrease in DEMG and PIIA. We suggest that cortical activity can explain persistency of active breathing during negative-pressure ventilation.     

Ventilatory and diaphragmatic EMG responses to negative-pressure ventilation in airflow obstruction

To assess the responses of patients with chronic obstructive lung disease (COLD) to negative-pressure ventilation (NPV), we studied eight naive patients with moderate to severe COLD before (control) and during NPV with "low" (-10-cmH2O) and "high" (-30-cmH2O) pressure swings in a Drinker tank respirator. Tidal volume (VT) and minute ventilation (VE) were recorded from a Respitrace and diaphragmatic electromyogram (DEMG) from a bipolar esophageal electrode. During short, 5-min runs of "low" and "high" NPV, VT did not change and VE increased in a borderline significant way at -30-cmH2O NPV. Peak integrated DEMG amplitude did not change with respect to control during short runs of NPV. However, when NPV was maintained for 20-60 min, a significant (though small, 20%) decrease in peak DEMG amplitude was observed with respect to control. By contrast, in a ninth patient habituated to NPV, the decrease in peak DEMG amplitude during a 5-min run of NPV was 60%. Significant increases in arterial PO2 (at -10- and -30-cmH2O NPV) and decreases in arterial PCO2 (at -30-cmH2O NPV) were found during NPV for the whole group of patients. One-to-one phase locking between the respirator and patients was the most common pattern of entrainment observed. However, 1:1 phase locking did not preclude the presence of dissociation between the two pacemakers. We conclude that short runs of NPV in naive patients do not result in changes in DEMG, as opposed to immediate and nearly complete cessation of inspiratory activity in trained patients.     

Reassessment of the interruption technique for measuring flow resistance in humans

We have previously produced evidence that, in patients with obstructive lung disease, compliance of extrathoracic airways is responsible for lack of mouth-to-alveolar pressure equilibration during respiratory efforts against a closed airway. The flow interruption method for measuring respiratory resistance (Rint) is potentially faced with the same problems. We reassessed the merits of the interruption technique by rendering the extrathoracic airways more rigid and by using a rapid shutter. We measured airway resistance (Raw) with whole body plethysmography during panting (at 2 Hz) and Rint during quiet breathing. Rint and Raw were expressed as specific airway (sGaw) and interruptive conductance (sGint), respectively. In nine healthy subjects (cheeks supported), sGint (0.140 +/- 0.050 s-1.cmH2O-1) was lower (P less than 0.02) than sGaw (0.182 +/- 0.043 s-1.cmH2O-1). By contrast, in 12 patients with severe obstructive lung disease (forced expiratory volume in 1 s/vital capacity = 41.0 +/- 19.8%), sGint (0.058 +/- 0.012 s-1.cmH2O-1) was higher (P less than 0.05) than sGaw (0.047 +/- 0.007 s-1.cmH2O-1), when the cheeks were supported. When the mouth floor was also supported, average values of sGaw (0.048 +/- 0.008 s-1.cmH2O-1) and sGint (0.049 +/- 0.014 s-1.cmH2O-1) became similar. In conclusion, we confirm previous findings in healthy subjects of higher values of Rint, with respect to Raw, probably because of differences in glottis opening between quiet breathing and panting. In airflow obstruction, supporting both the cheeks and the mouth floor decreased sGint, which became similar to sGaw.     

An elevated level of cholesterol impairs self-assembly of pulmonary surfactant into a functional film

In adult respiratory distress syndrome, the primary function of pulmonary surfactant to strongly reduce the surface tension of the air-alveolar interface is impaired, resulting in diminished lung compliance, a decreased lung volume, and severe hypoxemia. Dysfunction coincides with an increased level of cholesterol in surfactant which on its own or together with other factors causes surfactant failure. In the current study, we investigated by atomic force microscopy and Kelvin-probe force microscopy how the increased level of cholesterol disrupts the assembly of an efficient film. Functional surfactant films underwent a monolayer-bilayer conversion upon contraction and resulted in a film with lipid bilayer stacks, scattered over a lipid monolayer. Large stacks were at positive electrical potential, small stacks at negative potential with respect to the surrounding monolayer areas. Dysfunctional films formed only few stacks. The surface potential of the occasional stacks was also not different from the surrounding monolayer. Based on film topology and potential distribution, we propose a mechanism for formation of stacked bilayer patches whereby the helical surfactant-associated protein SP-C becomes inserted into the bilayers with defined polarity. We discuss the functional role of the stacks as mechanically reinforcing elements and how an elevated level of cholesterol inhibits the formation of the stacks. This offers a simple biophysical explanation for surfactant inhibition in adult respiratory distress syndrome and possible targets for treatment.     

Hypopharyngeal and neck cross-sectional changes monitored by inductive plethysmography

We present a method to assess cross-sectional area (CSA) changes of the extrathoracic airways (EA) by using an inductive plethysmograph (IP) band placed around the upper part of the neck. Measurements of mouth pressure (Pm) (or flow rate, V) and neck CSA changes during respiratory efforts against a high (or infinite) resistance have shown a highly significant relationship between Pm changes (or V changes, respectively), reflecting CSA changes of the EA and CSA changes of the neck. Simultaneous measurements of CSA of the neck (by IP) and of EA (by computerized tomography) during sustained inspiratory and expiratory efforts against a closed airway showed a high correlation between changes in the former and latter structures. Changes in CSA of the neck were larger with positive than negative transmural pressures, in keeping with the known larger compliance of this airway during expiration. We found this method helpful to assess the behavior of the EA during obstructive apnea episodes, hypopneas, and snoring.     

Wheat seed ageing viewed through the cellular redox environment and changes in pH

To elucidate biochemical mechanisms leading to seed deterioration, we studied 23 wheat genotypes after exposure to seed bank storage for 6–16 years compared to controlled deterioration (CD) at 45?°C and 14 (CD14) and 18% (CD18) moisture content (MC) for up to 32 days. Under two seed bank storage conditions, seed viability was maintained in cold storage (CS) at 0?°C and 9% seed MC, but significantly decreased in ambient storage (AS) at 20?°C and 9% MC. Under AS and CS, organic free radicals, most likely semiquinones, accumulated, detected by electron paramagnetic resonance, while the antioxidant glutathione (GSH) was partly lost and partly converted to glutathione disulphide (GSSG), detected by HPLC. Under AS the glutathione half-cell reduction potential (E_GSSG/2GSH) shifted towards more oxidising conditions, from ?186 to ?141?mV. In seeds exposed to CD14 or CD18, no accumulation of organic free radicals was observed, GSH and seed viability declined within 32 and 7 days, respectively, GSSG hardly changed (CD14) or decreased (CD18) and E_GSSG/2GSH shifted to ?116?mV. The pH of extracts prepared from seeds subjected to CS, AS and CD14 decreased with viability, and remained high under CD18. Across all treatments, E_GSSG/2GSH correlated significantly with seed viability (r?=?0.8, p<.001). Data are discussed with a view that the cytoplasm is in a glassy state in CS and AS, but during the CD treatments, underwent transition to a liquid state. We suggest that enzymes can be active during CD but not under the seed bank conditions tested. However, upon CD, enzyme-based repair processes were apparently outweighed by deteriorative reactions. We conclude that seed ageing by CD and under seed bank conditions are accompanied by different biochemical reactions.     

Airway closure in humans does not result in overestimation of plethysmographic lung volume

Exercise Physiol. 52: 638-641, 1982) have shown in dogs that airway closure may induce rib cage deformation and nonhomogeneous alveolar pressure swings, and they have suggested that this could lead to thoracic gas volume (TGV) overestimation by body plethysmography. However, in humans the rib cage is less easy to distort than in dogs. In four healthy volunteers we measured TGV by plethysmography before (B) and during (D) the occlusion of the middle and lower right lobes by a balloon (attached to a double-lumen catheter) positioned in the intermediate right bronchus. Subjects were trained to perform panting maneuvers preferentially with intercostals and accessory muscles or the diaphragm. Five to eleven TGV measurements were made in each subject with each panting pattern B and D occlusion. Balloon inflation resulted in no change in TGV whether low [13.3 +/- 3.4 (SD) cmH2O] or high (46.8 +/- 8.4 cmH2O) transdiaphragmatic pressures (Pdi) were used: TGV 4.0 +/- 0.4 (B) vs. 4.0 +/- 0.4 liters (D) and 4.3 +/- 0.4 (B) vs. 4.3 +/- 0.4 liters (D) for low and high Pdi, respectively. Thus, in trained subjects performing maneuvers aimed to distort the rib cage, no pressure difference was observed between the occluded and the nonoccluded lung during panting against the closed shutter. We conclude that it is unlikely that the mechanism proposed by Brown et al. might explain errors in lung volume measurements by body plethysmography in humans.