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C W Zwillich

Publications and source records attributed to C W Zwillich.

At least 19 recordsLinked to original sources
PubMed1992

Ventilatory response to sustained eucapnic hypoxia in the adult conscious dog.

The ventilatory response to 20 min sustained isocapnic hypoxia (SaO2, 80 +/- 2%) was examined in 5 trained unanesthetized adult dogs breathing through an endotracheal tube. End tidal PCO2 was maintained at the resting levels. The dogs' conscious status was monitored by recording EEG and EOG on a chart recorder. The room temperature was kept between 19 and 21 degrees C. All tests were repeated in each dog on 2 occasions: (1) unloaded tracheal breathing or (2) resistive loaded breathing. During unloaded tracheal breathing, the average ventilation in response to sustained hypoxia rose from a control of 5.1 +/- 0.3 L/min (mean +/- within-dog SE) to 19.2 +/- 1.1 L/min at the initial stage of hypoxia. Ventilation remained at 20.7 +/- 1.3 L/min at 10 min, and then 19.7 +/- 1.4 L/min at the completion of the 20 min hypoxic exposure. There was no ventilatory adaptation observed (P greater than 0.05). After release from hypoxia, the ventilation fell abruptly to 7.6 +/- 0.8 L/min, which was higher than the resting baseline level (P less than 0.05), and then gradually returned to the resting baseline within 10 min. Experiments exposing the dogs to 40 min sustained hypoxia also failed to elicit significant adaptation. During resistive loading, the pattern of average ventilation in response to sustained hypoxia was similar to that observed in unloaded breathing tests. But the ventilatory recovery was longer than unloaded breathing, returning to the resting baseline within 20 min. Again, there was no ventilatory adaptation observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1992

Adenosine infusion and periodic breathing during sleep.

Intravenously administered adenosine may increase ventilation (VI) and the ventilatory response to CO2 (HCVR). Inasmuch as we have previously hypothesized that those with higher HCVR may be more prone to periodic breathing during sleep, we measured VI and HCVR and monitored ventilatory pattern in seven healthy subjects before and during an infusion of adenosine (80 micrograms.kg-1.min-1) during uninterrupted sleep. Adenosine increased the mean sleeping VI (7.6 +/- 0.4 vs. 6.5 +/- 0.4 l/min, P less than 0.05) and decreased mean end-tidal CO2 values (42.4 +/- 1.2 vs. 43.7 +/- 1.0 Torr, P = 0.06, paired t test) during stable breathing. In six of seven subjects, periodic breathing occurred during this infusion. The amplitude (maximum VI--mean VI) and period length of this periodic breathing was variable among subjects and not predicted by baseline HCVR [correlation coefficients (r) = 0.64, P = 0.17 and r = -0.1, P = 0.9, respectively]. Attempts to measure HCVR during adenosine infusion were unsuccessful because of frequent arousals and continued periodic breathing despite hyperoxic hypercapnia. We conclude that adenosine infusion increases VI and produces periodic breathing during sleep in most normal subjects studied.

Adenosine↗
PubMed1992

Increased normoxic ventilation induced by repetitive hypoxia in conscious dogs.

To determine if a long-lasting increase in normoxic ventilatory drive is induced in conscious animals by repetitive hypoxia, we examined the normoxic [arterial O2 saturation (SaO2) > 93%] ventilatory response following successive episodes of 2-min eucapnic hypoxic challenges (SaO2 = 80%) in awake tracheotomized dogs. End-tidal CO2 was maintained at the resting level during and after repetitive hypoxia. The experimental protocol was performed twice in each of five dogs on separate days. To determine if changes in normoxic ventilation occurred between episodes of repetitive hypoxia, data were compared from six periods (epochs) for all experiments. The mean minute ventilation (VI) during three normoxic periods between episodes of intermittent hypoxia was 135, 154, and 169% of control (P < 0.05). VI during a 30-min recovery period was still higher at 183 and 172% of control (P < 0.05). Normoxic VI between hypoxic and recovery periods was significantly higher than the corresponding values in sham experiments. Our results indicate that a long-lasting increase in normoxic ventilation can be evoked in an awake unanesthetized dog by a short exposure to repetitive hypoxia.

Animals↗
PubMed1992

Adenosine stimulation, ventilation, and arousal from sleep.

The mechanism for arousal from sleep resulting from respiratory stimuli is unclear. We hypothesized that arousal is a result of increasing ventilation during sleep. To determine if this is true we compared minute ventilation at the point of arousal from non-REM sleep produced by the respiratory stimulant adenosine to that resulting from progressive hypercapnic stimulation. If this hypothesis is correct, the quantity of breathing immediately preceding arousal from sleep should be similar for each stimulus. We monitored electroencephalogram (EEG), electromyogram (EMG), end-tidal CO2, and inspired minute ventilation (VI) in five healthy young men during full-night sleep studies. Sleep state was monitored during the baseline state, during an intravenous infusion of 80 micrograms/kg/min of adenosine, and during multiple trials of progressive hyperoxic hypercapnia. Arousal from sleep occurred in association with increased breathing 4.2 +/- 1.1 times during adenosine infusion, 2.0 +/- 0 times during hypercapnic stimulation, and 4.0 +/- 0.6 times in the absence of stimulated breathing (spontaneously) per subject. Minute ventilation for the breath preceding arousal associated with adenosine stimulation (13.0 +/- 1.4 L/min) was similar to that preceding arousal caused by hypercapnia (12.9 +/- 1.1 L/min). In each case this level of breathing was greater than that preceding spontaneously occurring arousals (8.2 +/- 1.1 L/min), p less than 0.05). Although variable between subjects, there was a high correlation for these two variables within subjects (R = 0.96, p = 0.01). These data support the hypothesis that increasing ventilation induces arousal from sleep when ventilation is increased regardless of the stimulus producing this rising drive to breathe.

Adenosine↗
PubMed1992

The effect of repeat action albuterol sulfate (Proventil Repetabs) in nocturnal symptoms of asthma.

At four medical centers, 98 patients with stable asthma, histories of nighttime awakening at least three times weekly and nighttime declines of pulmonary function of at least 15%, who were not taking oral adrenergic agonists, were randomly treated with either oral repeat-action albuterol sulfate (Proventil Repetabs), 4 mg in the morning and 4-16 mg at bedtime, or a placebo for 2 weeks. All patients were required to have nocturnal symptoms of asthma, with prior use of bronchodilators other than oral adrenergic agonists to be eligible for the study. The patients maintained a diary of asthma symptom scores and recorded peak flow rates at home at bedtime and in the morning. They had spirometry (FEV1, FVC, and PEFR) after a 1-week baseline stabilization period, and after 1 and 2 weeks of double-blind oral therapy as noted above. Efficacy was evaluated by changes in the bedtime and morning peak flow rates, changes in the number of nighttime awakenings, results of office spirometry testing, and by physician and patient global evaluations of response to therapy. Of the 98 patients in the study, 47 received oral albuterol, and 51 received placebo. The patients on albuterol had a statistically significant reduction in the number of nighttime awakenings (p less than or equal to 0.01), as compared with the patients on placebo; this included both the average number of awakenings per week (p = 0.04), and the mean number of nights with awakenings per week (p = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Effect of oxygen breathing following submaximal and maximal exercise on recovery and performance.

To determine whether supplemental oxygen following exercise hastens recovery or enhances subsequent performance we evaluated its effectiveness in 13 male athletes. The exercise periods consisted of two 5-min submaximal efforts on a treadmill ergometer followed by a single bout to exhaustion. Intervals of exercise were separated by a 4-min recovery period during which the subject breathed either 1) room air, 2) 100% oxygen, or 3) 2 min of 100% oxygen followed by 2 min of room air on three nonconsecutive days. We found that breathing 100% oxygen produced no significant difference on the recovery kinetics of minute ventilation or heart rate, or improvement in subsequent performance as measured by duration of exercise (3.33 +/- 0.04 min, air vs 3.46 +/- 0.03, oxygen) and peak VO2 (59.9 +/- 2.2 ml.kg-1.min-1, air vs 54.5 +/- 2.2, oxygen). In addition, the perceived magnitude of exertion estimated by the Borg scale was no different during oxygen breathing. These findings offer no support for the use of supplemental oxygen in athletic events requiring short intervals of submaximal or maximal exertion.

Adult↗
PubMed1991

Changes in upper airway muscle activation and ventilation during phasic REM sleep in normal men.

Several investigators have observed that irregular breathing occurs during rapid-eye-movement (REM) sleep in healthy subjects, with ventilatory suppression being prominent during active eye movements [phasic REM (PREM) sleep] as opposed to tonic REM (TREM) sleep, when ocular activity is absent and ventilation more regular. Inasmuch as considerable data suggest that rapid eye movements are a manifestation of sleep-induced neural events that may importantly influence respiratory neurons, we hypothesized that upper airway dilator muscle activation may also be suppressed during periods of active eye movements in REM sleep. We studied six normal men during single nocturnal sleep studies. Standard sleep-staging parameters, ventilation, and genioglossus and alae nasi electromyograms (EMG) were continuously recorded during the study. There were no significant differences in minute ventilation, tidal volume, or any index of genioglossus or alae nasi EMG amplitude between non-REM (NREM) and REM sleep, when REM was analyzed as a single sleep stage. Each breath during REM sleep was scored as "phasic" or "tonic," depending on its proximity to REM deflections on the electrooculogram. Comparison of all three sleep states (NREM, PREM, and TREM) revealed that peak inspiratory genioglossus and alae nasi EMG activities were significantly decreased during PREM sleep compared with TREM sleep [genioglossus (arbitrary units): NREM 49 +/- 12 (mean +/- SE), TREM 49 +/- 5, PREM 20 +/- 5 (P less than 0.05, PREM different from TREM and NREM); alae nasi: NREM 16 +/- 4, TREM 38 +/- 7, PREM 10 +/- 4 (P less than 0.05, PREM different from TREM)]. We also observed, as have others, that ventilation, tidal volume, and mean inspiratory airflow were significantly decreased and respiratory frequency was increased during PREM sleep compared with both TREM and NREM sleep. We conclude that hypoventilation occurs in concert with reduced upper airway dilator muscle activation during PREM sleep by mechanisms that remain to be established.

Adult↗
PubMed1990

Upper airway resistance and geniohyoid muscle activity in normal men during wakefulness and sleep.

Sleep-related reduction in geniohyoid muscular support may lead to increased airway resistance in normal subjects. To test this hypothesis, we studied seven normal men throughout a single night of sleep. We recorded inspiratory supraglottic airway resistance, geniohyoid muscle electromyographic (EMGgh) activity, sleep staging, and ventilatory parameters in these subjects during supine nasal breathing. Mean inspiratory upper airway resistance was significantly (P less than 0.01) increased in these subjects during all stages of sleep compared with wakefulness, reaching highest levels during non-rapid-eye-movement (NREM) sleep [awake 2.5 +/- 0.6 (SE) cmH2O.l-1.s, stage 2 NREM sleep 24.1 +/- 11.1, stage 3/4 NREM sleep 30.2 +/- 12.3, rapid-eye-movement (REM) sleep 13.0 +/- 6.7]. Breath-by-breath linear correlation analyses of upper airway resistance and time-averaged EMGgh amplitude demonstrated a significant (P less than 0.05) negative correlation (r = -0.44 to -0.55) between these parameters in five of seven subjects when data from all states (wakefulness and sleep) were combined. However, we found no clear relationship between normalized upper airway resistance and EMGgh activity during individual states (wakefulness, stage 2 NREM sleep, stage 3/4 NREM sleep, and REM sleep) when data from all subjects were combined. The timing of EMGgh onset relative to the onset of inspiratory airflow did not change significantly during wakefulness, NREM sleep, and REM sleep. Inspiratory augmentation of geniohyoid activity generally preceded the start of inspiratory airflow. The time from onset of inspiratory airflow to peak inspiratory EMGgh activity was significantly increased during sleep compared with wakefulness (awake 0.81 +/- 0.04 s, NREM sleep 1.01 +/- 0.04, REM sleep 1.04 +/- 0.05; P less than 0.05). These data indicate that sleep-related changes in geniohyoid muscle activity may influence upper airway resistance in some subjects. However, the relationship between geniohyoid muscle activity and upper airway resistance was complex and varied among subjects, suggesting that other factors must also be considered to explain sleep influences on upper airway patency.

Adult↗
PubMed1990

Geniohyoid muscle activity in normal men during wakefulness and sleep.

Reduction in the activity of upper airway "dilator" muscles during sleep may allow the pharyngeal airway to collapse in some individuals. However, quantitative studies concerning the effect of sleep on specific upper airway muscles that may influence pharyngeal patency are sparse and inconclusive. We studied seven normal men (mean age 27, range 22-37 yr) during a single nocturnal sleep study and recorded sleep staging parameters, ventilation, and geniohyoid muscle electromyogram (EMGgh) during nasal breathing throughout the night. Anatomic landmarks for placement of intramuscular geniohyoid recording electrodes were determined from a cadaver study. These landmarks were used in percutaneous placement of wire electrodes, and raw and moving-time-averaged EMGgh activities were recorded. Sleep stage was determined using standard criteria. Stable periods of wakefulness and non-rapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep were selected for analysis. The EMGgh exhibited phasic inspiratory activity during wakefulness and sleep in all subjects. In six of seven subjects, mean and peak inspiratory EMGgh activities were significant (P less than 0.05) reduced during stages 2 and 3/4 NREM sleep and REM sleep compared with wakefulness. This reduction of EMGgh activity was shown to result from a sleep-related decline in the level of tonic muscle activity. Phasic inspiratory EMGgh activity during all stages of sleep was not significantly different from that during wakefulness. Of interest, tonic, phasic, and peak EMGgh activities were not significantly reduced during REM sleep compared with any other sleep stage in any subject. In addition, the slope of onset of phasic EMGgh activity was not different during stage 2 NREM and REM sleep compared with wakefulness in these subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

The influence of increasing ventilatory effort on arousal from sleep.

Arousal from sleep in response to asphyxia can be a lifesaving event. However, the mechanisms responsible for this important arousal response are uncertain. A unifying hypothesis is that arousal results from the increased respiratory effort that occurs as a result of ventilatory stimulation. If this is true, the magnitude of this effort during the breaths immediately preceding arousal from sleep should be similar regardless of the stimulus. Therefore, the negative inspiratory pleural pressure during the breaths preceding arousal would be similar, whether stimulated by added inspiratory resistive load, hypoxia, or hypercapnia. To test this hypothesis, we studied eight young, healthy men during full-night sleep studies. We measured their electroencephalography (EEG), electromyography (EMG), electrooculography (EOG), inspired ventilation (VI), end tidal PCO2 (PETCO2), O2 saturation, and esophageal pressure (esophageal balloon) while inducing arousal from non-REM sleep using (1) a 30-cm H2O/L/s added resistive load, (2) progressive hypoxia, and (3) progressive hyperoxic hypercapnia. All subjects were eventually aroused following the addition of the 30-cm H2O/L/s added load and during progressive hypercapnia. However, only six of the eight men were aroused when the O2 saturation was reduced to a minimum of 70%. For each stimulus, arousal occurred at very different levels of ventilation and arterial chemistry (SaO2 and CO2). However, ventilatory effort for each subject was similar at the point of arousal regardless of the stimulus. The peak-negative esophageal pressure for the single inspiration preceding arousal (for the six subjects arousing with all three stimuli) was 16.8 +/- 1.4 cm H2O for added resistive load, 15.0 +/- 2.4 cm H2O for hypoxia, and 14.7 +/- 2.1 cm H2O for hypercapnia. We conclude that increasing ventilatory effort may be the stimulus to arousal from sleep independent of the source of this rising drive to breathe.

Adult↗
PubMed1990

Pulmonary function in obstructive sleep apnea. Relationships to pharyngeal resistance and cross-sectional area.

Reduction in the size of the pharynx and increased pharyngeal airflow resistance have been demonstrated in patients with obstructive sleep apnea (OSA). We evaluated 15 men with severe OSA and 10 nonapneic control subjects matched for age and weight in order to determine if PCSA, inspiratory pharyngeal airflow resistance, and abnormal breathing events during sleep were associated with alterations in the flow-volume relationship and other awake PFTs. Pharyngeal cross-sectional area was determined by CT, and pharyngeal resistance between choanae and epiglottis was measured during quiet awake breathing. In patients with OSA, there was an inverse relationship between the mean cross-sectional area of the oropharynx and the ratio of FEF50%/FIF50% (rs = -0.54; p = 0.03). In all subjects, pharyngeal resistance was inversely related to percentage of predicted values for FEF25-75% (rs = -0.56; p = 0.01). The frequency of apneas during sleep was significantly (p less than 0.05) related to the percentage of predicted values for MVV, TLC, FVC, and PIF. Obesity appears to account for the strength of these relationships. Flow-volume loops and other PFTs did not distinguish patients with OSA from controls.

Airway Resistance↗
PubMed1990

Dyspnea in the patient with chronic obstructive pulmonary disease. Etiology and management.

We have summarized much of the known information regarding the pathogenesis of dyspnea in the COPD patient and have reviewed a great many of the therapeutic options that have been investigated. It should be obvious that we are really in the early stages of our understanding about this symptom, and that we know very little about how to decide which treatment options are likely to succeed in any individual. At this time, there is no substitute for a careful assessment of each treatment modality that is instituted using a measurement tool, and the value of a comprehensive assessment as outlined cannot be overemphasized.

Anti-Anxiety Agents↗
PubMed1989

State-dependent hypotonia in posterior cricoarytenoid muscles of the larynx caused by cholinoceptive reticular mechanisms.

The neural control of the accessory respiratory muscles regulating upper airway patency is poorly understood. This is particularly true with regard to the declines in electromyographic (EMG) activity of upper airway muscles during sleep. To specify the cellular mechanisms causing decreased upper airway muscle tone during sleep, we used an established pharmacological model of rapid eye movement (REM) sleep. With this model, a REM sleep-like state was reliably produced by microinjecting the cholinergic agonist carbachol directly into the pontine reticular formation of the cat. EMG recording were taken from the posterior cricoarytenoid (PCA) muscles of the larynx during wakefulness and the carbachol-induced, REM sleep-like state. This experimental model had not been previously used to study the neuropharmacological control of the upper airway. The results revealed a dose-dependent decrease in PCA muscle tone caused by pontine microinjections of carbachol. To investigate the cholinergic specificity of these effects, the muscarinic cholinergic antagonist pirenzepine was centrally administered before carbachol. Pirenzepine pretreatment effectively blocked the carbachol-induced, REM sleep-like state and attendant changes in muscle tone. These results specify for the first time that muscarinic cholinergic mechanisms within the pontine reticular formation can causally mediate state-dependent hypotonia in accessory respiratory muscles of the upper airway.

Animals↗
PubMed1989

Collapsibility of the human upper airway during normal sleep.

Upper airway resistance (UAR) increases in normal subjects during the transition from wakefulness to sleep. To examine the influence of sleep on upper airway collapsibility, inspiratory UAR (epiglottis to nares) and genioglossus electromyogram (EMG) were measured in six healthy men before and during inspiratory resistive loading. UAR increased significantly (P less than 0.05) from wakefulness to non-rapid-eye-movement (NREM) sleep [3.1 +/- 0.4 to 11.7 +/- 3.5 (SE) cmH2O.1-1.s]. Resistive load application during wakefulness produced small increments in UAR. However, during NREM sleep, UAR increased dramatically with loading in four subjects although two subjects demonstrated little change. This increment in UAR from wakefulness to sleep correlated closely with the rise in UAR during loading while asleep (e.g., load 12: r = 0.90, P less than 0.05), indicating consistent upper airway behavior during sleep. On the other hand, no measurement of upper airway behavior during wakefulness was predictive of events during sleep. Although the influence of sleep on the EMG was difficult to assess, peak inspiratory genioglossus EMG clearly increased (P less than 0.05) after load application during NREM sleep. Finally, minute ventilation fell significantly from wakefulness values during NREM sleep, with the largest decrement in sleeping minute ventilation occurring in those subjects having the greatest awake-to-sleep increment in UAR (r = -0.88, P less than 0.05). We conclude that there is marked variability among normal men in upper airway collapsibility during sleep.

Adult↗
PubMed1989

Chemosensitivity and the ventilatory response to airflow obstruction during sleep.

There is an accumulating body of evidence which suggests that chemical control of breathing can play a role in destabilizing respiratory rhythm during sleep. We hypothesized that the sleeping ventilatory response to hypercapnia (HCVR) and/or hypoxia (HVR) would predict respiratory events following release of inspiratory airway obstruction (IAO) in normal men during non-rapid-eye-movement (NREM) sleep. We therefore measured HCVR, HVR, and ventilation for three breaths preceding and eight breaths following three totally obstructed inspirations in eight normal subjects during NREM sleep. After IAO, we generally observed transient hyperventilation that resulted in hypocapnia and prolonged expiratory time. We found the initial increase in inspiratory minute ventilation (VI) following IAO to be correlated with HCVR (r = 0.72, P less than 0.05) but not HVR. In addition, the maximum decrease in PCO2 below base line was also related to HCVR (r = 0.83, P less than 0.05). This decrement in PCO2 predicted the subsequent prolongation in expiratory time (TE, r = 0.83, P less than 0.05) that was frequently observed. HCVR tended to predict the prolongation of TE, at the nadir of CO2 (r = 0.69, P = 0.057). In conjunction with this hypocapnia and prolongation of TE, hypoventilation with falling VI was often observed followed by periodic hyper- and hypoventilation. These results suggest that high HCVR may result in ventilatory overshoot following IAO and may contribute to ventilatory instability during sleep.

Airway Obstruction↗
PubMed1989

Nocturnal asthma therapy. Inhaled bitolterol versus sustained-release theophylline.

Many asthmatics complain of increased symptoms, awakenings, and need for additional medications during the sleeping hours. Sustained-release theophylline (THEO) may be superior to conventional inhaled bronchodilators in preventing nocturnal asthma symptoms and the early morning decrement in lung function common to this population. However, recent studies have demonstrated that THEO may delay sleep onset and perturb sleep stage distribution. No previous study has evaluated electroencephalographic, cardiac, and gas exchange indices during sleep in asthmatics treated with THEO compared with a long-acting inhaled beta 2-agonist. The study goals were to determine if theophylline perturbed sleep when compared with beta 2-agonists and to determine which agent achieved best control of daytime and nocturnal pulmonary symptoms and lung dysfunction. We evaluated 26 subjects with mild to moderate asthma and a history of frequent nocturnal symptoms who previously demonstrated decrements in AM lung function. THEO was compared with 3 puffs every 8 h (6 A.M., 2 P.M., and 10 P.M.) of bitolterol (BITOL), a long-acting beta 2-agonist, in a randomized, double-blind, placebo-controlled cross-over study. Each drug was administered for a 2-wk period ending with two consecutive nights of sleep evaluation followed by cross-over to the alternate drug regimen. During THEO administration, plasma concentrations on awakening were 11.4 +/- 0.69 micrograms/ml as compared with 0.00 micrograms/ml during BITOL. THEO was not found to disrupt sleep as sleep latency, total sleep time, percentage of total sleep time spent in Stages 1, 2, and 3/4 and in REM sleep were similar during each regimen.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1989

Morphology of the uvula in obstructive sleep apnea.

Alterations in pharyngeal structure and function are considered fundamental in the pathogenesis of obstructive sleep apnea (OSA). However, little is known about morphologic features of the pharynx in patients with OSA. We therefore studied the tissue composition of the uvula (midsagittal section) in patients with OSA, using a quantitative, morphometric point-counting technique. Uvula tissue was obtained by uvulopalatopharyngoplasty (UPPP) in 33 patients (mean number of apneas per hour of sleep = 32.7 +/- 5.2) and by autopsy in 22 normal subjects not known to have OSA. All statistical comparisons were controlled for differences caused by age and body mass index. Patients with OSA had a significantly greater percentage of muscle in the uvula (18.1 +/- 1.9% versus 9.3 +/- 2.1%, p = 0.02) than did normal subjects. A significant difference in fat content was also found (9.5 +/- 1.4% in patients versus 4.0 +/- 1.0% in normal subjects, p less than 0.02). These differences between patients with OSA and control subjects could not be accounted for by anthropometric or sex differences. The percentage of uvula fat tissue was significantly related to the frequency of apneas and hypopneas in sleep (r = 0.43, p less than 0.01). Uvula morphology in 6 nonapneic snorers undergoing UPPP was similar to that of patients with OSA. We conclude that the uvula in patients with OSA contains more muscle and fat than the uvula in control subjects, possibly contributing to pharyngeal narrowing in OSA.

Female↗