The diagnosis of sleep apnea: questionnaires and home studies.

Alternatives to the standard method of diagnosing sleep apnea (SA) are becoming increasingly popular due to the expense and/or. In some cases, the limited availability of polysomnography (PSG). The most common diagnostic alternatives have been clinical prediction rules and portable monitoring. Most portable monitors record one or more signals such as oxygen saturation, heart rate, airflow, or ribcage and abdominal movements. To date, most published studies of these monitors have had serious methodologic problems that have limited the acceptance of this technology. We have developed a two-step diagnostic approach for SA based on a clinical prediction rule and the results from a simple, but reliable and accurate, portable monitor that records oxygen saturation, snoring, and body position. The preliminary results indicate that such a strategy is very useful in a population of outpatients suspected of having SA and would preclude the need for PSG to investigate for this possibility in the majority of patients. However, before portable monitoring becomes widely adopted, each system should be more thoroughly tested, and increased attention should be directed at the design of the study so that the results are more generalizeable to other sleep clinic populations.

Static properties of the passive pharynx in sleep apnea.

Complete paralysis under general anesthesia allowed separating anatomic factors from neural factors which influence pharyngeal patency. We compared static mechanical properties of the passive pharynx in normals and sleep apneics. The passive pharynx was narrower and more collapsible in sleep apneics than normal controls indicating significance of anatomic factors in the pathogenesis of obstructive sleep apnea.

Treatment, airway and compliance effects of a titratable oral appliance.

STUDY OBJECTIVES: To measure the effects of a titratable anterior mandibular repositioner on airway size and Obstructive Sleep Apnea (OSA) and to evaluate its compliance. DESIGN: Before and after insertion sleep studies were obtained in a total of 38 OSA patients of varying severity from three different sites. Covert compliance was measured by means of a newly-developed, miniaturized, temperature-sensitive, imbedded monitor. Validity testing was completed in six adult volunteers who wore monitors imbedded into small acrylic appliances. MEASUREMENTS AND RESULTS: The mean RDI before treatment was 32.6 (SEM 2.1) and after the insertion of the appliance, the RDI was reduced to 12.1 (SEM 1.7, p<0.001). RDI was reduced to less than 15/hour in 80% of a group of moderate OSA patients (RDI 15 to 30) and in 61% of a group of severe OSA patients (RDI > 30) with respect to baseline RDI. Fiber optic video endoscopy was performed on 9 OSA patients with and without the appliance. No significant differences in hypopharynx or oropharynx cross sectional areas were found, but at the level of the velopharynx, the airway size was significantly increased (p<0.05). The index of agreement was 0.99 between the monitor clock time and the subject's log sheets. Compliance data from eight OSA subjects instructed to wear the appliance during sleep indicated that it was worn for a mean of 6.8 hours with a range of 5.6 to 7.5 hours per night. CONCLUSION: The titratable adjustable mandibular advancement appliance, made from thermoelastic acrylic, significantly reduces RDI in moderate to severe OSA patients, has a direct effect on airway size and is well worn throughout the night.

Sleeping and breathing.

Breathing is controlled by an automatic brain-stem controller acted on by higher neural influences that stabilize breathing and compensate for neuromechanical abnormalities. Loss of this wakefulness-dependent descending influences during nonrapid eye movement (NREM) sleep results in the appearance of a hypocapnic apnea threshold, which is associated with periodic breathing when the gain of chemical feedback loops is high. In addition, loss of the descending wakefulness influence leads to loss of motor compensation that results in a rise in upper airway resistance, obstructive sleep apnea or hypoventilation in patients with kyphoskoliosis or thoracic neuromuscular disorders. REM sleep poses different problems for the respiratory control system owing to muscular atomia and suppression of chemical feedback. These changes are associated with respiratory deterioration in patients with compromised diaphragmatic function, eg, patients with chronic obstructive pulmonary disease.

Clinical conference in pulmonary disease. Factors influencing upper airway closure.

The factors which produce closure of the upper airway (UAW) in patients with the sleep apnea syndrome are still poorly understood. A distinction should be made between the factors which induce closure and those which reopen the UAW. Neurologic factors include arousal phenomena, the magnitude and timing of various motor outputs, and postsynaptic inhibition. Mechanical factors include the anatomy of the UAW, especially that above the tongue, the position of the neck and jaw, and mucosal adherence once occlusion has occurred. Muscle factors include the type of myosin isozyme, the forces generated by the large number of UAW muscles and the diaphragm, and the possibility of high-frequency fatigue occurring during occlusion. Hypoxia and acidosis probably play a critical role in making the UAW less stable. Currently, the best method to prevent UAW closure is by nasal CPAP. Patients with life-threatening arrhythmias due to sleep apnea should have a tracheostomy. The role of drugs is controversial. Respiratory or muscle stimulants should probably be avoided; oxygen, medroxyprogesterone, and protriptyline may be useful adjuncts.

Stimulation of vagal C-fibers alters timing and distribution of respiratory motor output in cats.

Pulmonary vascular congestion or pulmonary embolism in humans produces shallow tachypnea, and indirect experimental evidence suggests that this characteristic breathing pattern may result from activation of vagal unmyelinated afferents from the lung. We have investigated, in decerebrate cats, reflex changes in breathing pattern and in the activation of the diaphragm, posterior cricoarytenoid, and thyroarytenoid muscles caused by activating C-fiber afferents in the vagus nerve. The right vagus nerve was sectioned distal to the origin of the recurrent laryngeal nerve, eliminating vagal afferent traffic although preserving motor innervation of the larynx on that side. The left cervical vagus was stimulated electrically, and efferent activation of the laryngeal muscles was avoided by cutting the left recurrent laryngeal nerve. Transmission to the brain of vagal afferent traffic resulting from this stimulation was controlled by graded cold block of the nerve cranial to the site of application of the stimulus. Activation of C-fibers, when A-fibers were blocked, significantly decreased respiratory period and amplitude of diaphragm inspiratory burst. In addition, this selective activation of vagal C-fibers augmented postinspiratory activity of the diaphragm and recruited phasic expiratory bursts in the thyroarytenoid. We conclude that, in unanesthetized decerebrate cats, afferent traffic of vagal C-fibers initiates a pontomedullary reflex that increases respiratory frequency, decreases tidal volume, and augments braking of expiratory airflow.

Identification of a subsurface area in the ventral medulla sensitive to local changes in PCO2.

The exact location of the central respiratory chemoreceptors sensitive to changes in PCO2 has not yet been determined. To avoid the confounding effects of the cerebral circulation, we used the in vitro brain stem-spinal cord of neonatal rats (1-5 days old) to identify areas within 500 microns of the ventral surface of the medulla where changes in PCO2 evoked a sudden increase in the rate of respiratory neural activity. The preparation was superfused with mock cerebrospinal fluid (CSF) while maintained at constant temperature (26 +/- 1 degrees C) and pH (7.34). Respiratory frequency increased linearly with decreases in superfusate pH (r2 = 0.92, P less than 0.001), indicating that the respiratory circuitry for the detection of CO2 and stimulation of breathing was intact in this preparation. The search for central chemoreceptors was performed with a specially designed micropipette that allowed microejection of 2-10 nl of mock CSF equilibrated with different CO2-O2 gas mixtures. The pipette was advanced in 50- to 100-microns steps by use of a microdrive to a maximum depth of 500 microns from the surface of the ventral medulla. Depending on the location of the micropipette, ejection of CO2-acidified mock CSF at depths of 100-350 microns below the ventral surface of the medulla stimulated neural respiratory output. Using this response as an indication of the location of central respiratory chemoreceptors, we found that chemoreceptive elements were located in a column in the ventromedial medulla extending from the hypoglossal rootlets caudally to an area 0.75 mm caudal to VI nerve in the rostral medulla.(ABSTRACT TRUNCATED AT 250 WORDS)

Temporal changes in effectiveness of an inspiratory inhibitory electrical pontine stimulus.

We determined the temporal changes in effectiveness of inspiratory-shortening expiratory-prolonging stimulus trains delivered in the region of the nucleus parabrachialis medialis and compared the responses to those observed during trains delivered to the vagus in the same animals (pentobarbital, sodium-anesthetized paralyzed cats). The inspiratory inhibitory effect of the pontine stimulus was assessed from the effect the stimulus has on threshold for terminating inspiration. Stimulus effect increased gradually, reached a peak at 0.2-0.4 s, and declined thereafter. The time of occurrence of peak effect was different from that observed in the course of vagal stimulus trains. With long stimulus trains (19-40 s), the initial effect on inspiratory duration (TI) (i.e., shortening) rapidly subsided and, in six of eight animals, was replaced by TI prolongation. The initial effect on expiratory duration (TE) (i.e., prolongation) also gradually declined with time but TE remained above control throughout. The time constant of adaptation was very similar with vagal and pontine stimulus trains (12.2 and 11.0 s, respectively), but the gain of the adapting response was much more pronounced with pontine stimuli, resulting in a paradoxical effect while stimulation continued. We conclude that the response to pontine stimuli, as with vagal stimuli, displays both integrative and adaptive characteristics. The similarity of the time constants for vagal and pontine adaptation responses suggests that these two inputs share common processing pathways.

Effects of hypoxia on metabolic rate of conscious adult cats during cold exposure.

Oxygen consumption (VO2) and shivering movements were recorded in adult, conscious cats in a thermoneutral (24-27 degrees C) and in a cold (3-8 degrees C) environment during normoxia, hypoxia, or hyperoxia for 55 min. In the cold environment, VO2 correlated with shivering index (SI) under conditions of normoxia or ambient hypoxia (FIO2 = 0.12). During normoxia, VO2 was 63% higher in the cold than the thermoneutral environment. Ambient hypoxia acutely reduced VO2 in cold and thermoneutral environments, the decrement being greater for the former than the latter. Similarly, the variation in VO2 for unit change in SI was greater in hypoxia than normoxic conditions, suggesting that hypoxia influenced nonshivering as well as shivering components of cold-induced VO2. Hypoxia induced by CO (FICO = 0.002) also reduced VO2 and SI, a result that is consistent with previous results indicating that carotid body chemoreceptors do not mediate the suppression of shivering by ambient hypoxia. Hyperoxia increased VO2 and SI in the cold, and the effects of both hypoxia and hyperoxia in the cold were antagonized by increasing FICO2 to 0.03. The results demonstrate that hypoxia suppresses VO2 in the cold by reducing the intensity of shivering and, probably, by an action on metabolic rate that is unrelated to cold-induced calorigenesis.

Evidence that glycine and GABA mediate postsynaptic inhibition of bulbar respiratory neurons in the cat.

Experiments were carried out on decerebrate cats to identify transsynaptic mediators of spontaneous postsynaptic inhibition of bulbar inspiratory and postinspiratory neurons. Somatic membrane potentials were recorded through the central micropipette of a coaxial multibarreled electrode. Blockers of type A gamma-aminobutyric acid (GABA-A) and glycine receptors were iontophoresed extracellularly from peripheral micropipettes surrounding the central pipette. Effective antagonism was demonstrated by iontophoresis of agonists with antagonists; application of strychnine antagonized the action of glycine but not GABA, and application of bicuculline antagonized the action of GABA but not glycine. In both types of neurons, iontophoresis of either antagonist depolarized the somatic membrane and increased input resistance throughout the respiratory cycle. Bicuculline preferentially depolarized the somatic membrane in both types of neurons during inactive phases. Strychnine increased the firing rate of inspiratory neurons during inspiration despite maintenance of somatic membrane potential at preiontophoresis levels. Tetrodotoxin reduced the effects of iontophoresed bicuculline and strychnine, suggesting that the action of the antagonists required presynaptic axonal conduction. The present results suggest that presynaptic release of both GABA and glycine contributes to tonic postsynaptic inhibition of bulbar respiratory neurons. GABA-A receptors appear to contribute to inhibition during inactive phases in inspiratory and postinspiratory neurons, whereas glycinergic mechanisms appear to contribute to inspiratory inhibition in inspiratory neurons.

Hypoxia-induced changes in shivering and body temperature.

Experiments were carried out on conscious cats to evaluate the general characteristics and modes of action of hypoxia on thermoregulation during cold stress. Intact and carotid-denervated (CD) conscious cats were exposed to ambient hypoxia (low inspired O2 fraction) or CO hypoxia in prevailing laboratory (23-25 degrees C) or cold (5-8 degrees C) environments. In the cold, both groups promptly decreased shivering and body temperature when exposed to either type of hypoxia. Small increases in CO2 concentration reinstituted shivering in both groups. At the same inspired concentration of O2, CD animals decreased shivering and body temperature more than intact cats. While this difference resulted, in part, from a lower alveolar PO2 in CD cats, a difference between intact and CD cats was apparent when the two groups were compared at the same alveolar PO2. During more prolonged hypoxia (45 min), shivering returned but did not reach normoxic levels, and body temperature tended to stabilize at a hypothermic value. Exposure to various levels of hypoxia produced graded suppression of shivering, with the result that the change in body temperature varied directly with inspired O2 concentration. Hypoxia appears to act on the central nervous system to suppress shivering and sinus nerve afferents appear to counteract this direct effect of hypoxia. In intact cats, this counteraction appears to be sufficient to maintain body temperature under hypoxic conditions at room temperature but not in the cold.

Rapid shallow breathing caused by pulmonary vascular congestion in cats.

The vasculature of one lung of unanesthetized spontaneously breathing decerebrate cats was isolated and congested with blood. Such pulmonary vascular congestion (PVC) consistently resulted in a shallow tachypnea associated with expiratory activation of the diaphragm and thyroarytenoid muscles, signifying augmented expiratory braking. With progressive increases in pulmonary vascular pressure, tachypnea and expiratory braking increased progressively and ultimately obscured phasic activity in the diaphragm and thyroarytenoid. Thus the apnea caused by PVC constitutes not an arrest of neural respiratory activity but rather a continuous activation of thoracic inspiratory and laryngeal adductor muscles. When capsaicin, a neurotoxin that activates nonmyelinated afferents, was injected into the pulmonary artery of the isolated lung, it produced changes in timing and distribution of respiratory motor output that resembled those with PVC but were more abrupt in onset. Capsaicin, applied perineurally to the cervical vagi, preferentially blocked the conduction of nonmyelinated afferent fibers. This procedure, which produced little degradation in Hering-Breuer reflexes, eliminated tachypnea and expiratory braking caused by PVC or capsaicin injection. The results indicate that activation of pulmonary vagal afferent fibers of C or A-delta category in unanesthetized cats reflexly modifies the respiratory motor output in a way that resembles the human response to PVC or pulmonary embolism. This is a brain stem reflex.

Ventilatory responses to hypoxia and hypercapnia in awake rats pretreated with capsaicin.

Ventilatory responses to hypoxia and hypercapnia were measured by indirect plethysmography in unanesthetized unrestrained adult rats injected neonatally with capsaicin (50 mg/kg) or vehicle. Such capsaicin treatment ablates a subpopulation of primary afferent fibers containing substance P and various other neuropeptides. Ventilation was measured while the rats breathed air, 12% O2 in N2, 8% O2 in N2, 5% CO2 in O2, or 8% CO2 in O2. Neonatal treatment with capsaicin caused marked alterations in both the magnitude and composition of the hypoxic but not hypercapnic ventilatory response. The increase in minute ventilation evoked by hypoxia in the vehicle-treated rats resulted entirely from an increase in respiratory frequency. In the capsaicin-treated rats the hypoxic ventilatory response was significantly reduced owing to an attenuation of the frequency response. Although both groups responded to hypoxia with a shortening in inspiratory and expiratory times, rats treated with capsaicin displayed less shortening of both respiratory phases. By contrast, hypercapnia induced a brisk ventilatory response in the capsaicin-treated group that was similar in magnitude and pattern to that observed in the vehicle-treated group. Analysis of the components of the hypercapnic ventilatory responses revealed no significant differences between the two groups. We, therefore, conclude that neuropeptide-containing C-fibers are essential for the tachypnic component of the ventilatory response to hypoxia but not hypercapnia.

Estimating respiratory mechanics in the presence of flow limitation.

Dynamic collapse of the pulmonary airways, leading to flow limitation, is a significant event in a number of respiratory pathologies, including obstructive sleep apnea syndrome and chronic obstructive pulmonary disease. Quantitative evaluation of the mechanical status of the respiratory system in these conditions provides useful insights into airway caliber and tissue stiffness, which are hallmarks of such abnormalities. However, assessing respiratory mechanics in the presence of flow limitation is problematic because the single-compartment linear model on which most assessment methods are based is not valid over the entire breath. Indeed, even deciding which parts of a breath are flow limited from measurement of mouth flow and pleural pressure often proves to be difficult. In this study, we investigated the use of two approaches to assessing the overall mechanical properties of the respiratory system in the presence of inspiratory flow limitation. The first method is an adaptation of the classic Mead-Whittenberger method, and the second method is based on information-weighted histograms obtained from recursively estimated signals of respiratory resistance and elastance. We tested the methods on data simulated by using a computer model of the respiratory system and on data collected from obese sleeping pigs. We found that the information-weighted histograms provided the more robust overall estimates of respiratory mechanics.

Dynamic ventilatory response to CO(2) in congestive heart failure patients with and without central sleep apnea.

Nonobstructive (i.e., central) sleep apnea is a major cause of sleep-disordered breathing in patients with stable congestive heart failure (CHF). Although central sleep apnea (CSA) is prevalent in this population, occurring in 40-50% of patients, its pathogenesis is poorly understood. Dynamic loop gain and delay of the chemoreflex response to CO(2) was measured during wakefulness in CHF patients with and without CSA by use of a pseudorandom binary CO(2) stimulus method. Use of a hyperoxic background minimized responses derived from peripheral chemoreceptors. The closed-loop and open-loop gain, estimated from the impulse response, was three times greater in patients with nocturnal CSA (n = 9) than in non-CSA patients (n = 9). Loop dynamics, estimated by the 95% response duration time, did not differ between the two groups of patients. We speculate that an increase in dynamic gain of the central chemoreflex response to CO(2) contributes to the genesis of CSA in patients with CHF.

Interaction of cross-sectional area, driving pressure, and airflow of passive velopharynx.

Previous studies have shown that, when the pharyngeal muscles are relaxed, the velopharynx is a highly compliant segment of the pharynx. Thus, under these circumstances, cross-sectional area of the velopharynx (AVP), driving pressure across the velopharynx (DeltaP), and inspiratory airflow (VI) will be mutually interdependent variables. The purpose of the present investigation was to describe the interrelation among these three variables during inspiration. We studied 15 sleeping patients with obstructive sleep apnea/hypopnea when the pharyngeal muscles were rendered hypotonic by applying continuous positive airway pressure to the nasal airway. AVP, determined by endoscopic imaging, was significantly greater at onset of VI limitation than at minimum oropharyngeal pressure (P < 0. 01). Snoring was never observed during VI limitation. In a subgroup of six patients, values for DeltaP, VI, and AVP were obtained at 0. 1-s intervals at various levels of mask pressure. For these six patients, the mathematical expression VI = 0.657(AVP/Amax) . DeltaP0. 332, where Amax is maximal AVP, described the relationship among the three variables (R2 = 0.962) for flow-limited and non-flow-limited inspirations. The impedance of the passive velopharynx, defined as DeltaP0.33/V, was inversely related to AVP and increased dramatically when AVP was <0.3 cm2. In summary, we observed a progressive decrease in AVP during flow-limited inspiration in patients with obstructive sleep apnea. This constriction of the velopharynx contributes to an increase in velopharyngeal impedance that, in turn, counterbalances the increase in DeltaP during flow limitation.

Anatomy of pharynx in patients with obstructive sleep apnea and in normal subjects.

Anatomic abnormalities of the pharynx are thought to play a role in the pathogenesis of obstructive sleep apnea (OSA), but their contribution has never been conclusively proven. The present study tested this anatomic hypothesis by comparing the mechanics of the paralyzed pharynx in OSA patients and in normal subjects. According to evaluation of sleep-disordered breathing (SDB) by nocturnal oximetry, subjects were divided into three groups: normal group (n = 17), SDB-1 (n = 18), and SDB-2 (n = 22). The static pressure-area relationship of the passive pharynx was quantified under general anesthesia with complete paralysis. Age and body mass index were matched among the three groups. The site of the primary closure was the velopharynx in 49 subjects and the oropharynx in only 8 subjects. Distribution of the location of the primary closure did not differ among the groups. Closing pressure (PC) of the velopharynx for SDB-1 and SDB-2 groups (0.90 +/- 1.34 and 2.78 +/- 2.78 cmH2O, respectively) was significantly higher than that for the normal group (-3.77 +/- 3.44 cmH2O; P < 0.01). Maximal velopharyngeal area for the normal group (2.10 +/- 0.85 cm2) was significantly greater than for SDB-1 and SDB-2 groups (1.15 +/- 0.46 and 1.06 +/- 0.75 cm2, respectively). The shape of the pressure-area curve for the velopharynx differed between normal subjects and patients with SDB, being steeper in slope near Pc in patients with SDB. Multivariate analysis of mechanical parameters and oxygen desaturation index (ODI) revealed that velopharyngeal Pc was the only variable highly correlated with ODI. Velopharyngeal Pc was associated with oropharyngeal Pc, suggesting mechanical interdependence of these segments. We conclude that the passive pharynx is more narrow and collapsible in sleep-apneic patients than in matched controls and that velopharyngeal Pc is the principal correlate of the frequency of nocturnal desaturations.

Effects of vagal denervation on cardiorespiratory and behavioral responses in the newborn lamb.

Recently, Wong et al. (Wong KA, Bano A, Rigaux A, Wang B, Bharadwaj B, Schurch S, Green F, Remmers JE, and Hasan SU, J Appl Physiol 85: 849-859, 1998) demonstrated that fetal lambs that have undergone vagal denervation prenatally do not establish adequate alveolar ventilation shortly after birth. In their study, however, vagal denervation was performed prenatally and the deleterious effects of vagal denervation on breathing patterns and gas exchange could have resulted from the prenatal actions of the neurotomy. To quantify the relative roles of pre- vs. postnatal vagal denervation on control of breathing, we studied 14 newborn lambs; 6 were sham operated, and 8 were vagally denervated below the origin of the recurrent laryngeal nerve. Postoperatively, all denervated animals became hypoxemic and seven of eight succumbed to respiratory failure. In vagally denervated lambs, expiratory time increased, whereas respiratory rate, minute ventilation, and lung compliance decreased compared with the sham-operated animals. In the early postoperative period, the frequency of augmented breaths was lower but gradually increased over time in the denervated vs. sham-operated group. The dynamic functional residual capacity was significantly higher than the passive functional residual capacity among the sham-operated group compared with the denervated group. No significant differences were observed in the prevalence of various sleep states and in the amount of total phospholipids or large- and small-aggregate surfactants between the two groups. We provide new evidence indicating that intrauterine actions of denervation are not required to explain the effects of vagal denervation on postnatal survival. Our data suggest that vagal input is critical in the maintenance of normal breathing patterns, end-expiratory lung volume, and gas exchange during the early neonatal period.

Hypoxia similarly impairs metabolic responses to cutaneous and core cold stimuli in conscious rats.

Cold exposure elicits several thermoregulatory responses, including an increased metabolic heat production from shivering and nonshivering thermogenesis. The increased metabolism can be in response to body core and/or body cutaneous cooling. Hypoxic hypoxia has been shown to attenuate the metabolic response to cutaneous cooling. We measured metabolic heat production in adult conscious rats during independent cutaneous and core cooling, during normoxia and hypoxia, to 1) test the hypothesis that hypoxia suppresses the metabolic response to independent core cooling and 2) determine whether hypoxia acts preferentially on the response to cutaneous or core cooling. The animals were studied in a temperature-controlled metabolic chamber, and body core temperature was controlled by an abdominal heat exchange coil. Ambient temperature was varied (10, 19, and 28 degrees C) while core temperature was clamped at 37 degrees C or core temperature was varied (33, 35, and 37 degrees C) at a stable ambient temperature of 28 degrees C. Our data indicate that although the sensitivity of the metabolic response to core cooling is about five to six times that to cutaneous cooling. Hypoxia similarly attenuates thermoregulatory responses to both stimuli.

Monitoring respiratory function and sleep in the obese Vietnamese pot-bellied pig.

Development of drug treatments for obstructive sleep-disordered breathing has been impeded by the lack of animal models. The obese pig may be a suitable animal model, as it has been reported to experience sleep-disordered breathing resembling human obstructive sleep apnea. The purpose of this paper is to describe in detail techniques for chronic instrumentation of the obese Vietnamese pot-bellied pig and to study respiratory function during sleep. Under general anesthesia, four obese pigs were instrumented for long-term recording of intrapleural and tracheal pressures, genioglossal EMG, and bioelectric signals related to sleep. A custom-fitted face mask was used to record respiratory variables including airflow, snoring, and expired CO(2). Most chronic instrumentation provided robust signals for up to 6 wk after installation. All pigs displayed sleep-disordered breathing characterized by increased resistance to airflow, snoring, inspiratory flow limitation, and possible sleep disruption. Apneas and hypopneas were not a feature of breathing during sleep in these animals. Nonetheless, this animal preparation may be useful for exploring possible drug treatments for obstructive sleep-disordered breathing.