To evaluate the extent and nature of the variability of measurements of upper airway area by acoustic reflection (AAAR), we made repeated measures of pharyngeal AAAR in 10 normal adult volunteers. We selected mean pharyngeal area as a better index of upper airway size than peak pharyngeal area or pharyngeal volume. Within-run variability of this measure was 8 +/- 4% (SD) (coeff of variation). This variability could not be explained by changes in lung volume or differences in phase of respiration. Five subjects had tracheal and pharyngeal area measured by using both the custom-made wax mouthpiece (W) and a commercial rubber pulmonary function mouthpiece (R). Reproducibility of pharyngeal AAAR was within 10% (coeff of variation) using R, but measurements of pharyngeal AAAR varied with the different types of mouthpiece, as W/R ranged from 0.72 to 1.70. In contrast, measurements of midtracheal area were similar for both mouthpiece types [mean W/R = 0.97 +/- 14 (SD)]. The acoustic reflection technique yields a reproducible index of pharyngeal size that does not vary with phase of respiration or modest changes in lung volume. Either W or R may be used to make clinical measurements, but the type of mouthpiece should be consistent and specified.

This investigation used a previously described bench-top device (Gaver et al., J. Appl. Physiol. 69: 74-85, 1990) to examine the role of nonnewtonian and viscoelastic fluids on events at reopening of a closed flexible tube. Aqueous sodium alginate solutions with and without calcium chloride and sodium dodecyl sulfate in desired concentrations provided fluids with a wide range of surface tensions, storage and loss moduli, and nonnewtonian steady shear viscosity. Dimensionless analysis, using the shear rate-dependent viscosities, was applied to reduce reopening pressure-meniscus velocity data to a master curve. With regard to fluid properties, we found that 1) fluid elasticity strongly changes the pressure-velocity relationship, causing flow instability at higher meniscus velocities; 2) decreasing surface tension gives rise to a smaller yield pressure for reopening; and 3) whereas larger tubes are easier to open, smaller tubes produce additional shear thinning of the lining fluid. These results suggest that, for both the upper (large) and lower (small) airways, nonnewtonian and viscoelastic properties of the mucosal fluid modify the time of closure and rate of reopening.

Aims of this study: To determine the associations, if any, of cavernosal oxygen tension with vasculogenic impotence. Materials and Methods: We evaluated penile cavernosal blood gas levels in men with suspected vasculogenic impotence during penile duplex ultrasonography andaor dynamic infusion cavernosometry and cavernosography (DICC). Patients with suspected impotence were evaluated from 1992 ± 1996. Patient ages ranged from 24 ± 75 y (mean 48 y). Eighteen men had arteriogenic impotence diagnosed by abnormal penile duplex ultrasound after injection of a vasoactive agent, and 23 men had venous leakage diagnosed by DICC. Results: Eighteen men with arteriogenic impotence had the following mean blood gas values: pH 7.38 AE 0.01, PCO2 45.50 AE 0.94, PO2 65.17 AE 2.16. Twenty-three men with venogenic (venous leak) impotence had the following mean cavernosal blood gas values: pH 7.41 AE 0.01, PCO2 42.26 AE 0.83, PO2 74.17 AE 2.51. The differences in PO2 were signi®cant (P`0.05). A subgroup of men with severe venous leakage had PO2 values that were similar to the low arterial PO2 values. Conclusion: The low PO2 in patients with arteriogenic impotence, and the subset of men with severe venous leak impotence, support a global concept of low cavernosal PO2 as a mechanism for both arteriogenic and venogenic impotence.

Respiratory chemical and reflex interventions have been shown to affect nasal resistance or tracheal tone, respectively. In the present study, nasal caliber (assessed from pressure at a constant flow) and tracheal tone (assessed from pressure in a fluid-filled balloon within an isolated tracheal segment) were monitored simultaneously in anesthetized, paralyzed, artificially ventilated (inspired O2 fraction = 100%) cats. We examined the effect of CO2 inhalation and sciatic nerve stimulation as well as the application of nicotine (6 X 10(-4) mol/l) or lidocaine (2% solution) to the intermediate area of the ventral medullary surface (VMS). CO2 and VMS nicotine resulted in a significant increase in tracheal pressure [147 +/- 73 and 91 +/- 86% (SD), respectively]; and a significant reduction in nasal pressure (-35 +/- 10 and -20 +/- 13%, respectively). In contrast, sciatic nerve stimulation resulted in a significant fall in both tracheal (-50 +/- 36%) and nasal pressure (-21 +/- 13%). Application of 2 or 4% lidocaine to the VMS reduced tracheal pressure but did not significantly affect nasal pressure. After VMS lidocaine, nasal and tracheal responses to CO2, sciatic nerve stimulation, or VMS nicotine, when present, were negligible. These results suggest a role for the VMS in the regulation and coordination of nasal and tracheal caliber responses.

To examine the elastic behavior of the upper airway, we obtained pressure-area plots from data gathered from acoustic images of the airway and measurements of mouth pressure during tidal breathing in 10 adult human volunteers (dA/dP). These plots revealed both tidal hysteresis and a change in slope as a function of distance along the airway. The slope of the regression line of the dA/dP plots decreased from the pharyngeal region to the trachea and became 0 at the thoracic inlet, the location of which was independently assessed. In most subjects the slope became negative distal to the thoracic inlet. Correlation coefficients between pressure and area approached 1 in the pharyngeal region and 0 at the thoracic inlet. When subjects breathed against a small resistive load (10 cmH2O.1(-1).s) pharyngeal, extrathoracic, and intrathoracic pressure-area plots were exaggerated but the slope at the thoracic inlet was unchanged. We conclude that this pressure-area characteristic defines regional differences in upper airway elasticity and delineates the transition point between the intra- and extrathoracic airways.

The purpose of this study was to define the pathways and mechanisms involved in the neural regulation of laryngeal mucosal gland functions. In anesthetized, paralyzed, and artificially ventilated dogs, the responses of laryngeal submucosal glands to stimulation of laryngeal mechanoreceptors and peripheral chemoreceptors were examined by measuring the number of hillocks and volume of secreted fluid before and after activation of sensory nerve endings. Compared with a control period, the number of hillocks and volume of secreted fluid significantly increased (P < 0.05) with mechanical stimulation of the vocal folds (n = 13) and with chemical activation of peripheral chemoreceptors by systemic administration of sodium cyanide (100 micrograms/kg; n = 11). The reflex responses induced by vocal fold stimulation and activation of peripheral chemoreceptors were slightly decreased by interrupting transmission in the recurrent laryngeal nerves (P > 0.05) and were abolished by subsequent sectioning of superior laryngeal nerves or prior intravenous administration of atropine methylnitrate (P < 0.05). In denervated animals, topical application of nicotine on laryngeal epithelium caused significant activation of submucosal glands (P < 0.05). We conclude that laryngeal secretion can be significantly altered reflexly by stimulation of laryngeal sensory nerve endings and peripheral chemoreceptors, that both superior and recurrent laryngeal nerves convey cholinergic outflow to laryngeal submucosal glands, and that nicotine acting locally activates laryngeal submucosal glands.

Upper airway dilating muscle activity is characterized by an early-peaking pattern which serves to dilate or stiffen the upper airway at the time when the greatest negative intraluminal pressure is generated by contraction of chest wall muscles. This pattern has been attributed to phasic afferent inputs from pulmonary stretch receptors. The present study examines the hypothesis that nonvagal factors may also influence the discharge pattern and coordination of upper airway and chest wall muscle activities. Therefore, in anesthetized, paralyzed, vagotomized and artificially ventilated cats, we examined the effects of changes in respiratory drive produced by activation of cholinergic and GA-BAergic (γ-aminobutyric acid) receptors at the ventrolateral aspects of the medulla oblongata on phasic intrabreath discharge patterns of hypoglossal and phrenic nerves. Cholinergic agents (acetylcholine, carbachol, methacholine, physostigmine) applied directly to chemoreceptive areas on the ventral medullary surface increased hypoglossal activity, and in addition converted inspiratory discharge from an augmenting to a decrementing pattern of activity. The reverse effect on the discharge pattern of hypoglossal activity was observed with a decrease in respiratory drive. While the amplitude of the phrenic nerve discharge was also affected by these interventions, the augmenting discharge pattern of phrenic nerve activity did not change. These results suggest that the early peaking pattern of hypoglossal nerve discharge in vagotomized cats also depends on the level of respiratory drive, and is not solely dependent on vagal afferent inputs. In addition, the data suggest that structures near the ventral surface of the medulla are influential in shaping the pattern of hypoglossal nerve activity and maintaining balanced activity of upper airway and chest wall muscles.

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