scholarly journals The effect of inhaled menthol on upper airway resistance in humans: A randomized controlled crossover study

2013 ◽  
Vol 20 (1) ◽  
pp. e1-e4 ◽  
Author(s):  
Effie J Pereira ◽  
Lauren Sim ◽  
Helen S Driver ◽  
Chris M Parker ◽  
Michael F Fitzpatrick

BACKGROUND: Menthol (l-menthol) is a naturally-occurring cold receptor agonist commonly used to provide symptomatic relief for upper airway congestion. Menthol can also reduce the sensation of dyspnea. It is unclear whether the physiological action of menthol in dyspnea reduction is through its cold receptor agonist effect or whether associated mechanical changes occur in the upper airway.OBJECTIVE: To determine whether menthol inhalation alters upper airway resistance in humans.METHODS: A randomized, sham-controlled, single-blinded crossover study of inhaled menthol on upper airway resistance during semirecumbent quiet breathing in healthy subjects was conducted. Ten healthy participants (eight female) with a mean (± SD) age of 21±1.6 years completed the study.RESULTS: Nasal resistance before testing was similar on both occasions. No differences were found in respiratory frequency (mean ± SEM) (menthol 17.0±1.1 cmH2O/L/s; sham 16.9±0.9 cmH2O/L/s), minute ventilation (menthol 7.7±0.5 cmH2O/L/s; sham 7.9±0.5 cmH2O/L/s) or total inspiratory time/total breath time (menthol 0.4±0.1 cmH2O/L/s; sham 0.4±0.1 cmH2O/L/s). The upper airway resistance was similar during menthol (3.47±0.32 cmH2O/L/s) and sham (3.27±0.28 cmH2O/L/s) (P=0.33) inhalation.CONCLUSION: Inhalation of menthol does not alter upper airway resistance in awake human subjects.


1961 ◽  
Vol 16 (2) ◽  
pp. 326-330 ◽  
Author(s):  
Robert E. Hyatt ◽  
Roger E. Wilcox

Simultaneous extrathoracic and intrathoracic flow resistance was measured in 19 unanesthetized subjects during mouth breathing. Lateral intratracheal pressure was recorded from a needle introduced 2 cm below the larynx. The intratracheal-oral pressure gradient was recorded during various respiratory maneuvers. The pressure drop from esophagus to trachea was also recorded. The extrathoracic pressure-flow relationships were alinear. Large inter- and intrasubject variability in upper airway resistance was encountered. Some factors contributing to this variability were defined. The upper airway accounted for approximately 45% of the total airway resistance in nine normal and 20% in 10 emphysematous human subjects. Upper airway resistance decreased with increasing lung inflation in four normal subjects. The magnitude and potential variability of the upper airway resistance must be considered in evaluating maneuvers designed to alter intrathoracic flow resistance, especially in normal human beings. It appears that during mouth breathing the major component of the upper airway resistance is located in the larynx. Submitted on September 14, 1960



1990 ◽  
Vol 69 (2) ◽  
pp. 617-624 ◽  
Author(s):  
K. G. Henke ◽  
J. A. Dempsey ◽  
J. M. Kowitz ◽  
J. B. Skatrud

To determine the effects of the sleep-induced increases in upper airway resistance on ventilatory output, we studied five subjects who were habitual snorers but otherwise normal while awake (AW) and during non-rapid-eye-movement (NREM) sleep under the following conditions: 1) stage 2, low-resistance sleep (LRS); 2) stage 3-4, high-resistance sleep (HRS) (snoring); 3) with continuous positive airway pressure (CPAP); 4) CPAP + end-tidal CO2 partial pressure (PETCO2) mode isocapnic to LRS; and 5) CPAP + PETCO2 isocapnic to HRS. We measured ventilatory output via pneumotachograph in the nasal mask, PETCO2, esophageal pressure, inspiratory and expiratory resistance (RL,I and RL,E). Changes in PETCO2 were confirmed with PCO2 measurements in arterialized venous blood in all conditions in one subject. During wakefulness, pulmonary resistance (RL) remained constant throughout inspiration, whereas in stage 2 and especially in stage 3-4 NREM sleep, RL rose markedly throughout inspiration. Expired minute ventilation (VE) decreased by 12% in HRS, and PETCO2 increased in LRS (3.3 Torr) and HRS (4.9 Torr). CPAP decreased RL,I to AW levels and increased end-expiratory lung volume 0.25-0.93 liter. Tidal volume (VT) and mean inspiratory flow rate (VT/TI) increased significantly with CPAP. Inspiratory time (TI) shortened, and PETCO2 decreased 3.6 Torr but remained 1.3 Torr above AW. During CPAP (RL,I equal to AW), with PETCO2 returned to the level of LRS, VT/TI and VE were 83 and 52% higher than during LRS alone. Also on CPAP, with PETCO2 made equal to HRS, VT, VT/TI, and VE were 67, 112, and 67% higher than during HRS alone.(ABSTRACT TRUNCATED AT 250 WORDS)



1995 ◽  
Vol 79 (2) ◽  
pp. 411-419 ◽  
Author(s):  
A. Kay ◽  
J. Trinder ◽  
Y. Kim

Sleep-induced hypoventilation is caused partly by inadequate compensation for elevated upper airway resistance (UAR). Some evidence suggests that the effect of UAR on ventilation may vary among individuals. The relationship between minute ventilation (VI) and UAR was examined in 26 healthy young men (average of 10.12 sleep onsets). Variables were analyzed over transitions between wakefulness (defined by alpha electroencephalographic activity) and sleep (theta electroencephalographic activity). Transitions to sleep were associated with increases in UAR in synchrony with reductions in VI, and equally rapid opposite changes occurred with awakenings. The relationship between the magnitudes of the changes in VI and UAR at transitions varied among subjects, accounting for 30% of the variance for alpha-to-theta transitions and 50% of the variance for theta-to-alpha transitions. Results indicated that, although ventilatory changes during sleep onset are partly a consequence of changes in UAR, alterations in UAR do not account fully for alterations in VI. Other factors that may contribute to ventilatory instability during sleep onset include state-related fluctuations in drive to the primary respiratory muscles and variability in compensatory mechanisms.



1994 ◽  
Vol 77 (5) ◽  
pp. 2285-2290 ◽  
Author(s):  
D. W. Hudgel ◽  
H. B. Hamilton

During spontaneous sleep-induced periodic breathing in elderly subjects, we have found that tidal volume oscillations are related to reciprocal oscillations in upper airway resistance. The purpose of this study was to address the mechanism of the relationship between oscillations in tidal volume and upper airway resistance in elderly subjects with sleep-induced periodic breathing. We hypothesized that the spontaneous periodic breathing observed in non-rapid-eye-movement (NREM) sleep in elderly subjects would be closely related to fluctuations in upper airway resistance and not to changes in central motor drive to ventilatory pump muscles. Therefore, in eight healthy elderly subjects, we measured costal margin chest wall peak moving time average electrical inspiratory activity (CW EMG), ventilation variables, and upper airway resistance during sleep. Five of eight subjects had significant sine wave oscillations in upper airway resistance and tidal volume. For these five subjects, there was a reciprocal exponential relationship between peak upper airway inspiratory resistance and tidal volume or minute ventilation [r = -0.60 +/- 0.20 (SD) (P < 0.05) and -0.55 +/- 0.26 (P < 0.05), respectively], such that as resistance increased, ventilation decreased. The relationship between CW EMG and tidal volume or minute ventilation was quite low (r = 0.12 +/- 0.32 and -0.07 +/- 0.27, respectively). This study demonstrated that oscillations in ventilation during NREM sleep in elderly subjects were significantly related to fluctuations in upper airway resistance but were not related to changes in chest wall muscle electrical activity. Therefore, changes in upper airway caliber likely contribute to oscillations in ventilation seen during sleep-induced periodic breathing in the elderly.



1994 ◽  
Vol 77 (2) ◽  
pp. 856-861 ◽  
Author(s):  
F. G. Issa ◽  
S. Porostocky ◽  
T. Feroah

We investigated the effect of sleep and sighing on supratracheal resistance in unrestrained mongrel dogs breathing through the nose by comparing within-breath changes in upper airway pressure-flow relationship in control, sigh, and five postsigh breaths recorded during wakefulness and during non-rapid-eye-movement and rapid-eye-movement sleep. A sigh breath was characterized by a high tidal volume and was typically followed by an apnea of a variable duration. Sleep had little or no effect on supratracheal resistance, measured at peak flow rates, during quiet breathing (awake 7.3 +/- 0.4, non-rapid eye movement 8.3 +/- 0.4, and rapid eye movement 6.8 +/- 0.4 cmH2O.l–1.s). The resistance was identical in the early part of inspiration in control and sigh breaths but increased during the augmented phase of sigh breaths. Resistance at peak inspiratory flow was higher in sigh breaths than in control breaths in all sleep states. The flow-pressure profile of postsigh breaths was identical to that of control breaths in all sleep states. We conclude that upper airway resistance is essentially unaffected by sleep state in the mongrel dog and that sighing increases upper airway resistance regardless of sleep state.



1985 ◽  
Vol 58 (5) ◽  
pp. 1489-1495 ◽  
Author(s):  
J. P. Farber

The suckling opossum exhibits an expiration-phased discharge in abdominal muscles during positive-pressure breathing (PPB); the response becomes apparent, however, only after the 3rd-5th wk of postnatal life. The purpose of this study was to determine whether the early lack of activation represented a deficiency of segmental outflow to abdominal muscles or whether comparable effects were observed in cranial outflows to muscles of the upper airways due to immaturity of afferent and/or supraspinal pathways. Anesthetized suckling opossums between 15 and 50 days of age were exposed to PPB; electromyogram (EMG) responses in diaphragm and abdominal muscles were measured, along with EMG of larynx dilator muscles and/or upper airway resistance. In animals older than approximately 30 days of age, the onset of PPB was associated with a prolonged expiration-phased EMG activation of larynx dilator muscles and/or decreased upper airway resistance, along with expiratory recruitment of the abdominal muscle EMG. These effects persisted as long as the load was maintained. Younger animals showed only those responses related to the upper airway; in fact, activation of upper airway muscles during PPB could be associated with suppression of the abdominal motor outflow. After unilateral vagotomy, abdominal and upper airway motor responses to PPB were reduced. The balance between PPB-induced excitatory and inhibitory or disfacilitory influences from the supraspinal level on abdominal motoneurons and/or spinal processing of information from higher centers may shift toward net excitation as the opossum matures.



2008 ◽  
Vol 139 (4) ◽  
pp. 535-540 ◽  
Author(s):  
Chunli Gao ◽  
Liang Zhou ◽  
Chunsheng Wei ◽  
Matthew R. Hoffman ◽  
Cai Li ◽  
...  

Objective To measure the upper-airway resistance in patients with tracheostomies and determine the value representing decannulation readiness. Subjects and Methods Fifty-six patients with tracheostomies resultant to laryngeal disease participated in this study. Forty patients met clinical criteria for decannulation; 16 did not. Subglottal pressure was measured with a tube connected to the tracheostomy tube, and airflow was monitored simultaneously using a facemask. Upper-airway resistance measurements were recorded during shallow and deep breathing. Results During both shallow and deep breathing, the inspiratory and expiratory resistances were significantly higher for the group unsuitable for decannulation ( P < .0001). The areas under the receiver operating characteristic curves were 0.938 or greater for the four curves, indicating a high sensitivity and specificity of resistance measures for diagnosis. Conclusions Objective measurement of upper-airway resistance during shallow and deep breathing may be a useful parameter in determining decannulation readiness of tracheostomized patients.



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