Laryngeal-receptor responses to phasic CO2 in anesthetized cats

We compared the effects of CO2 applied continuously and during expiration on laryngeal-receptor activity in paralyzed, artificially ventilated and nonparalyzed, spontaneously breathing cats by using an isolated larynx, artificially ventilated to approximate a normal respiratory cycle. The majority of quiescent negative-pressure and all cold receptors were excited by 5 and 9% CO2 applied both continuously and during expiration. In general, quiescent positive-pressure, tonic negative-pressure, and tonic positive-pressure receptors were inhibited by 5 and 9% CO2 applied continuously and during expiration. There were no significant differences between responses to 5 and 9% CO2 or to continuous and expired CO2 or between paralyzed and nonparalyzed preparations. In conclusion, laryngeal receptors respond to changes in CO2 concentration occurring during a normal respiratory cycle. Because laryngeal-receptor stimulation exerts reflex effects on ventilation and upper airway muscle activity, these results suggest that airway CO2 plays a role in reflex regulation of breathing and upper airway patency.     

Neuronal gagging activity patterns may be generated by neurons in the reticular area dorsomedial to the retrofacial nucleus in dogs

Expulsion is induced when hypercapnea and hypoxia develop during retching, or when the oropharyngeal mucosa is irritated (the gag reflex). The central pattern generator (CPG) for expulsion has been suggested to coexist with the CPG for retching in the reticular area dorsomedial to the retrofacial nucleus, which may correspond to the Botzinger complex (BOT). However, its participation in gagging induced by oropharyngeal irritation is unclear. To elucidate such participation, the firing patterns of BOT neurons were observed during gagging induced by stimulation of superior laryngeal afferents in decerebrate, paralyzed dogs. Only 23% of inspiratory and 34% of expiratory BOT neurons increased their firing in response to stimulation of the superior laryngeal nerve. In contrast, 75% of nonrespiratory BOT neurons showed enhanced firing with this stimulation. During gagging, each nonrespiratory, inspiratory, and expiratory BOT neuron fired with the same pattern that they exhibited during expulsion caused by changes in blood gases. These firing patterns could be classified into five types and are thought to be appropriate for generating neuronal gagging activity. These results suggest that the CPG for expulsion in the BOT produces gagging when it is activated by oropharyngolaryngeal afferents.     

Upper airway reflexes during a combination of propofol and fentanyl anesthesia

BACKGROUND: The effects of intravenous anesthetics on airway protective reflexes have not been fully explored. The purpose of the present study was to characterize respiratory and laryngeal responses to laryngeal irritation during increasing doses of fentanyl under propofol anesthesia. METHODS: Twenty-two female patients anesthetized with propofol and breathing through the laryngeal mask airway were randomly allocated to three groups: (1) eight patients who received cumulative total doses of 200 microg fentanyl given in the form of two doses of 50 microg and one dose of 100 microg spaced 6 min under mechanical controlled ventilation while end-tidal carbon dioxide tension (PCO2) was maintained at 38 mmHg (fentanyl-controlled ventilation group), (2) eight patients who received cumulative total doses of 200 microg fentanyl while breathing spontaneously while end-tidal PCO2 was allowed to increase spontaneously (fentanyl-spontaneous ventilation group), and (3) six spontaneously breathing patients who were anesthetized with propofol alone (propofol group). The laryngeal mucosa of each patient was stimulated by spraying the cord with distilled water, and the evoked responses were assessed by analyzing the respiratory variables and endoscopic images. RESULTS: Before administration of fentanyl, laryngeal stimulation caused vigorous reflex responses, such as expiration reflex spasmodic panting, cough reflex, and apnea with laryngospasm. Increasing doses of fentanyl reduced the incidences of all these responses, except for apnea with laryngospasm, in a dose-related manner in both the fentanyl-controlled ventilation and the fentanyl-spontaneous ventilation groups. Detailed analysis of endoscopic images revealed several characteristics of laryngeal behavior during the airway reflex responses. CONCLUSION: Incremental doses of fentanyl depress airway reflex responses in a dose-related manner, except for apnea with laryngospasm.     

Activities of expiratory neurones of the B?tzinger complex during vocalization in decerebrate cats

Repetitive electrical stimulation of the midbrain peri-aqueductal grey (PAG) terminates quiet breathing and initiates inspiration that precedes vocalization. To understand the neuronal mechanisms underlying this phenomenon, activities of expiratory neurones (n = 39) of the B?tzinger complex (BOT) were examined in decerebrate cats. Most augmenting expiratory (E-aug) neurones (20/22) of the BOT, including 15 bulbospinal neurones, decreased their activities (9/20) or ceased to discharge (11/20) after the onset of stimulation of the PAG. This suggests that suppression of E-aug neurones of the BOT, which project to phrenic motoneurones, results in disinhibition of these neurones, and, in turn, terminates expiration and initiates inspiration preceding vocalization.     

Effect of upper airway cooling and CO2 on diaphragm and geniohyoid muscle activity in the rat

Upper airway (UA) reflexes play an important role in regulating breathing and UA patency, but the effects of UA CO2 and cooling on ventilation and UA muscle activity are controversial. Diaphragm and geniohyoid electromyographic activities were recorded in anaesthetized rats, breathing spontaneously through a low-cervical tracheostomy. Warmed, humidified air containing 0 or 10% CO2 and cooled, room humidity air were applied at constant flow to the UA through a high- cervical tracheostomy. Spontaneous tracheal airflow, UA airflow and temperature, blood pressure, and rectal temperature were recorded. In all animals, the geniohyoid muscle had phasic inspiratory activity, which slightly preceded diaphragmatic activity. CO2 had no effect on mean peak integrated diaphragmatic activity and variable effects on geniohyoid activity. The coefficients of variation of these activities were unaffected by CO2. Similar results were obtained following bilateral mid-cervical vagotomy. Cool air decreased respiratory frequency (78+/-8%) (mean+/-SD % of control), peak inspiratory flow (78+/-5%) and diaphragmatic activity (77+/-4%), and increased geniohyoid activity (149+/-11%). Cutting the superior laryngeal nerves abolished these effects. In conclusion, whilst moderate upper airway cooling inhibits breathing and excites geniohyoid muscle activity, upper airway carbon dioxide has minimal effect.     

Influence of upper airway pressure changes on respiratory frequency

Influences of pressure changes within the upper airway on respiratory frequency were studied in anesthetized rabbits. These reflex effects were investigated in two ways: (1) by applying sustained negative or positive pressures to isolated upper airway in vagally intact animals during tracheostomy breathing, and (2) by briefly occluding the nasal airways of vagotomized animals at end expiration. Negative pressure applied to isolated upper airway decreased the respiratory frequency (P less than 0.01). Decrease in respiratory frequency correlated with magnitude of pressure change. In contrast, positive pressures produced an increase in respiratory frequency (P less than 0.05). But, the increase in frequency correlated poorly with magnitude of positive pressure change. A post-stimulus effect lasting several breaths was seen following the release of both negative and positive pressures (P less than 0.01). Nasal occlusion in vagotomized animals was associated with an increase in Ti and Ttot of the first nasally occluded breath (P less than 0.05). Increase in Ti was not associated with an increase in peak diaphragmatic activity. This would result in decreased inspiratory load on the upper airway patency maintaining muscles by reducing the mean inspiratory pressure. Hence, these reflex responses to airway pressure could play a functional role in the maintenance of upper airway patency.     

Locally administered vascular endothelial growth factor cDNA increases survival of ischemic experimental skin flaps

Both end-inspiratory (EIO) and end-expiratory (EEO) airway occlusions are used to calculate the strength of the Hering-Breuer inflation reflex (HBIR) in infants. However, the influence of the timing of such occlusions is unknown, as is the extent to which changes in volume within and above the tidal range affect this reflex. The purpose of this study was to compare both techniques and to evaluate the volume dependency of the HBIR in healthy, sleeping infants up to 1 yr of age. The strength of the HBIR was expressed as the ratio of expiratory or inspiratory time during EIO or EEO, respectively, to that recorded during spontaneous breathing, i.e., as the "inhibitory ratio" (IR). Paired measurements of the EIO and EEO in 26 naturally sleeping newborn and 15 lightly sedated infants at approximately 1 yr showed no statistically significant differences in the IR according to technique: mean (95% CI) of the difference (EIO - EEO) being -0.02 (-0.17, 0.13) during the first week of life and 0.04 (-0.14, 0.22) at 1 yr. During tidal breathing, a volume threshold of approximately 4 ml/kg was required to evoke the HBIR. Marked volume and age dependency were observed. In newborn infants, occlusions at approximately 10 ml/kg during sighs always resulted in an IR > 4, whereas a similar response was only evoked at 25 ml/kg in older infants. Age-related changes in the volume threshold may reflect maturational changes in the control of breathing and respiratory mechanics throughout the first year of life.     

Relationship between velopharyngeal dimensions and palatal EMG during progressive hypercapnia

To examine the contribution of specific palatal muscles to velopharyngeal dimensions, we recorded electromyographic (EMG) activity in the levator veli palatini, the tensor veli palatini, and the palatoglossus while examining the velopharynx (VP) with videoendoscopy in eight awake normal adults. Simultaneous display of VP images and airflow provided precise timing of events. Video images and EMG signals were recorded during progressive hypercapnia. Every tenth breath was analyzed. For each selected breath, VP area, anteroposterior and lateral diameters, and EMG activity were determined at five points: beginning, middle, and end of inspiration and middle and end of expiration. VP measurements changed significantly during the respiratory cycle. Although maximum area was measured at end inspiration or middle expiration and minimum area at the beginning or end of the breath, respiratory-related changes in VP measurements and EMG activity were characterized by substantial inter- and intrasubject variability. This variability is similar to velopharyngeal behavior during nonrespiratory tasks and suggests that upper airway patency is determined by multiple factors.     

Detection of nivalenol genotoxicity in cultured cells and multiple mouse organs by the alkaline single-cell gel electrophoresis assay

The effects of upper airway (UAW) flows and pressures on breathing pattern and respiratory muscle activities were studied in anesthetized rats breathing through a tracheostomy. A steady flow (approximately 1000 ml/kg/min) of cold dry air, or cold wet air, or warm wet air was passed through the UAW, in the expiratory direction for approximately 20 sec (20-40 sec). In other trials positive or negative pressure was applied to the isolated UAW for a similar duration. There was a marked prolongation of the expiratory duration and decreases in peak inspiratory flow, tidal volume, and peak diaphragm electromyogram (EMG) activity in response to cold dry airflow. The responses to cold wet air were reduced but still significant. Warm wet air had no effect on breathing. These responses show that UAW cooling and drying depress breathing in the rat and that cooling itself could cause the inhibition of breathing. Negative pressure induced substantial increases in genioglossus and laryngeal inspiratory activity while positive pressure caused a decrease in genioglossus activity. Positive pressure also increased expiratory time while negative pressure increased inspiratory time. These results confirm the functional role of the UAW dilating muscles in preventing UAW from collapse in rats.     

Comparison of unilateral arytenoid lateralization and ventral ventriculocordectomy for the treatment of experimentally induced laryngeal paralysis in dogs

This study evaluated changes in respiratory function in dogs with experimentally induced laryngeal paralysis treated with either unilateral arytenoid lateralization or ventral ventriculocordectomy, and compared the effectiveness of these procedures. Evaluation consisted of clinical assessment and tidal breathing flow volume loop and upper airway resistance measurements. Carbon dioxide and doxapram hydrochloride were used as respiratory stimulants. Initially, all dogs improved clinically after corrective surgery. However, by the end of the study, laryngeal collapse had developed in 2 of 5 dogs corrected by ventral ventriculocordectomy. No statistical differences in upper airway mechanics testing were seen between the surgical procedures. With both groups combined, many measurements of upper airway obstruction improved after surgical correction. Based on this study, these surgical procedures yield comparable results, although additional studies are needed to evaluate both the cause of laryngeal collapse and the role of upper airway mechanics testing in the evaluation of canine laryngeal paralysis.     

Pulmonary function measurements during repeated environmental challenge of horses with recurrent airway obstruction (heaves)

OBJECTIVES: To evaluate the degree of reproducibility in clinical variables, blood gas measurements, and lung function variables, and the changes in these variables caused by exposure to moldy hay in naturally sensitized and control horses. PROCEDURE: The magnitude of variation in arterial blood gas and pulmonary function measurements were evaluated in a model of naturally acquired heaves. Horses with heaves and similarly aged control horses were studied prior to moldy hay challenge and again after the horses with heaves manifested clinical signs of airway obstruction. This cycle of testing was repeated 3 times to determine the variation of the before and after challenge measurements. Variables evaluated for repeatability included: clinical score; arterial O2 and CO2 tensions; pulmonary function variables, such as breathing rate (f), tidal volumes, and flow rates; lung resistance (RL); dynamic compliance; and work of breathing (Wb). RESULTS: Before challenge, significant differences observed between control horses and horses with heaves included clinical score, expiratory flow rate at near-end expiration, RL, and Wb. After exposure to moldy hay, variables measured in control horses were largely unchanged. However, in the afflicted horses, significant changes were observed for clinical score, arterial O2 and CO2 tensions, breathing rate, peak tidal inspiratory and expiratory flow rates, dynamic compliance, RL, and Wb, compared with prechallenge values and with control horses' postchallenge values. Analysis of the data revealed few statistically significant differences between repeats of challenges. CONCLUSION: Horses afflicted with heaves manifest airway obstruction that can be measured in repeatable fashion.     

Reduction of 4-cyclohexyl-1-[(1R)-1,2-diphenylethyl]-piperazine-induced memory impairment of passive avoidance performance by sigma 1 receptor agonists in mice

The laryngeal chemoreflex (LCR) is a potentially life-threatening reflex that is elicited in immature animals by the topical application of water to the laryngeal mucosa. The reflex response is characterized by immediate apnea and laryngeal adduction and delayed cardiovascular instability. The cardiorespiratory changes of the LCR may be life-threatening, particularly in very immature animals such as piglets under 2 weeks of age. The afferent and efferent limbs of the LCR are mediated through the vagus nerve, but the neuromediators responsible for the reflex changes have not yet been clearly elucidated. Previous agonist and antagonist studies in immature dogs demonstrated that substance P, a sensory tachykinin, mediates the life-threatening esophagolaryngeal adductor reflex elicited by distal esophageal sensory nerve stimulation. This study was conducted to determine if substance P also plays a role in mediating the LCR. The LCR response was compared before and after treatment with intravenous substance P antagonist (Pfizer CP-96,345-1) in eight piglets (mean 27.7 days of age). The laryngeal and cardiovascular responses of the animals following intravenous administration of the tachykinins substance P, neurokinin A, and neurokinin B were also assessed. Pretreatment with substance P antagonist did not alter the LCR's duration of apnea (p > .10), laryngeal adductor response, or early change in mean arterial pressure (p > .10), although the early maximal heart rate response was significantly altered (p < .01). Intravenous substance P, neurokinin A, and neurokinin B did not reproduce the laryngeal respiratory response of the LCR. We conclude that substance P, neurokinin A, and neurokinin B are not key neurotransmitters of the LCR.     

Effects of NREM sleep on dynamic within-breath changes in upper airway patency in humans

The purpose of our study was to compare inspiratory- and expiratory-related changes in retropalatal cross-sectional area (CSA) during wakefulness to those during non-rapid-eye-movement (NREM) sleep. We studied 18 subjects in whom the severity of sleep-disordered breathing varied. Relative changes in CSA were visualized by using fiber-optic endoscopy. For each breath analyzed (wakefulness n = 4-13; sleep n = 7-16), the CSA was measured at fixed points within inspiration and expiration (0, 25, 50, and 100% of the inspiratory and expiratory duration); these measurements were expressed as a percentage of the CSA that occurred at the start of inspiration. During wakefulness, there was a statistically significant increase in the retropalatal CSA (compared with the start of inspiration) only during early expiration (group mean: expiration, 0% = 112.6 +/- 3.2 (SE) %; 25% = 122.8 +/- 6.2%; 50% = 110.6 +/- 3.8%). In contrast, during sleep, significant changes in CSA occurred during both inspiration and expiration (group mean: inspiration, 25% = 75.3 +/- 6.0%; 50% = 66.7 +/- 7.7%; 75% = 64.6 +/- 8.1%; expiration, 0% = 126.8 +/- 11.8%; 25% = 125.3 +/- 6.9%). The expiratory-related increase in CSA was followed by narrowing such that at end expiration the caliber of the airway was returned to that occurring at the beginning of inspiration (group mean at end expiration = 98.6 +/- 3.1%). The largest changes in CSA occurred in the subjects with an increased body mass index (BMI). We conclude that, during NREM sleep, significant changes in CSA occur during both inspiration and expiration and that the magnitude of these changes is significantly influenced by BMI.     

Laryngeal and abdominal muscle electrical activity during periodic breathing in nonsedated lambs

We recently reported that glottic closure was present throughout central apneas in awake lambs. The present study tested whether glottic closure was also observed during periodic breathing (PB). We attempted to induce PB in 21 nonsedated lambs on return from hypocapnic hypoxia to room air. Airflow and thyroarytenoid (a laryngeal constrictor, n = 16), cricothyroid (a laryngeal dilator, n = 10), and abdominal (n = 9) muscle electrical activity (EMG) were monitored continuously. PB was observed in 16 lambs, with apneic phases in 8 lambs. Thyroarytenoid muscle EMG was observed at the nadir of PB, either throughout apnea or with prolonged expiration during the lowest respiratory efforts. Phasic inspiratory cricothyroid muscle EMG and phasic expiratory abdominal EMG disappeared at the nadir of PB. Active glottic closure at the nadir of PB, without abdominal muscle contraction, could be a beneficial mechanism, preserving alveolar gas stores for continuing gas exchange during the apneic/hypopneic phase of PB. However, consequences of active glottic closure on ventilatory instability, either enhancing or reducing, are unknown.     

Opinion of the people in charge of the medical graduation disciplines at the S?o Paulo University Medical School on the ''curriculum evaluation program''

Several studies were focused on the consequences of reduced PaO2 (hypoxemia) on the Breuer-Hering inspiration-inhibiting vagal reflex. However, these data are often contradictory and do not allow us to decide whether hypoxemia interacts with the central integration of pulmonary vagal afferents and/or exerts peripheral influence on pulmonary stretch receptor (PSR) activity. The present study was performed in anesthetized rabbits breathing different gas mixtures containing O2, N2 and CO2. Intravenous injection of bicarbonates and CO2 addition in the inspired mixture maintained pHa and PaCO2 within their physiological ranges. The Breuer-Hering reflex, assessed from the changes in diaphragmatic EMG activity, was elicited either by inflating the lungs at different volumes above the functional residual capacity (PSR activation) or by direct electrical stimulation of vagal afferents (central stimulation). Hypoxemia never significantly modified the strength of the reflex or its threshold. Thus, acute hypoxemia present at high altitude does not seem to modify the key role played by PSR afferents in the ventilatory control.     

Reflex relationships between the cervical esophagus and the respiratory system in cats

The present study focused on reflex relationships between the esophagus and the respiratory system in cats, namely the changes in airway tone and pulmonary circulation elicited by mechanical or acid (pH 2) stimulation of esophageal afferents. One-minute of sustained distension of the cervical esophagus increased tracheal pressure (PTr), decreased pulmonary artery pressure (PPA) and to a higher extent pulmonary blood flow (QPA) and lowered arterial blood pressure (Pa). This was associated with significant variations in arterial blood gases (increased PaO2 and decreased PaCO2). Acid stimulation of the cervical esophagus caused a marked increase in PTr and a modest fall in QPA. In both circumstances, cervical bivagotomy abolished PTr changes, whereas the changes in pulmonary hemodynamics but not in Pa were then accentuated. Further cervical sympathectomy suppressed the vascular response. These observations show the existence of reflex influences of esophageal afferents on the control of airway tone and pulmonary vascular resistance. The vagus nerve is the efferent arm of the bronchomotor reflex whereas modulation of the sympathetic control of pulmonary circulation seems to be responsible for the changes in pulmonary hemodynamics.     

A systems analysis approach to medical error

Using decerebrate frogs (Rana catesbeiana), we investigated the role of vagal and laryngeal sensory feedback in controlling motor activation of the larynx. Vagal and laryngeal nerve afferents were activated by electrical stimulation of the intact vagal and laryngeal nerves. Pulmonary afferents were activated by lung inflation. Reflex responses were recorded by measuring efferent activity in the laryngeal branch of the vagus (Xl) and changes in glottal aperture. Two glottic closure reflexes were identified, one evoked by lung inflation or electrical stimulation of the main branch of the vagus (Xm), and the other by electrical stimulation of Xl. Lung inflation evoked a decrementing burst of Xl efferent activity and electrical stimulation of Xm resulted in a brief burst of Xl action potentials. Electrical stimulation of Xl evoked a triphasic mechanical response, an abrupt glottal constriction followed by glottal dilatation followed by a long-lasting glottal constriction. The first phase was inferred to be a direct (nonreflex) response to the stimulus, whereas the second and third represent reflex responses to the activation of laryngeal afferents. Intracellular recordings of membrane potential of vagal motoneurons of lung and nonlung types revealed EPSPs in both types of neurons evoked by stimulation of Xm or Xl, indicating activation of glottal dilator and constrictor motoneurons. In summary, we have identified two novel reflexes producing glottic closure, one stimulated by activation of pulmonary receptors and the other by laryngeal receptors. The former may be part of an inspiratory terminating reflex and the latter may represent an airway protective reflex.     

Immediate response to inspiratory resistive loading in anesthetized patients with kyphoscoliosis: spirometric and neural effects

In kyphoscoliosis (KS), lung volumes are reduced, respiratory elastance and resistance are increased, and breathing pattern is rapid and shallow, attributes that may contribute to defense of tidal volume (VT) in the face of inspiratory resistive loading. The control of ventilation of 12 anesthetized patients about to undergo corrective spinal surgery was compared to that of 11 anesthetized patients free of cardiothoracic disease during quiet breathing and the first breath through one of three linear resistors. Mean forced vital capacity (FVC) of the KS group was 48% that of the controls (C). Passive elastance (Ers) and active elastance and resistance (E'rs and R'rs, respectively) were computed according to previously described techniques (Behrakis PK, Higgs BD, Baydur A, Zin WA, Milic-Emili J (1983) Active inspiratory impedance in halothane-anesthetized humans. J Appl Physiol 54: 1477-1481). Baseline tidal volume VT, inspiratory duration Tl, expiratory duration TE, duration of total breathing cycle TT, and inspiratory duty cycle TI/TT were significantly reduced, while VE was slightly decreased in the KS. Ers, E'rs, and R'rs, were, respectively, 72, 69, and 89% greater in the KS. Driving pressure (Pmus) was derived from the equation of motion, using active values of respiratory elastance. With resistive loading, there was greater prolongation of TI in the C, while percent reduction in VT and minute ventilation VE was less in KS. Compensation in both groups was achieved through three changes in the Pmus waveform. (1) Peak amplitude increased. (2) The duration of the rising phase increased. (3) The rising Pmus curve became more concave to the time axis. These changes were most marked with application of the highest resistance in both groups. Peak driving pressure and mean rate of rise of Pmus were greater in the KS. Increased intrinsic impedance, Pmus, and differences in changes in neural timing in anesthetized kyphoscoliotics contribute to modestly greater VT defense, compared to that of anesthetized subjects free of cardiorespiratory disease.     

Habituation to intense acoustic stimulation during cortical spreading depression in rats

We have studied the pattern of breathing before, during and after augmented breaths in spontaneously breathing, anesthetized cats with the larynx both in and out of the breathing circuit. Following augmented breaths we consistently observed increases in end-expiratory lung volume (EEV), end-expiratory transpulmonary pressure, dynamic lung compliance and respiratory frequency. These changes were of similar magnitude whether the larynx was in or out of circiut and were uninfluenced by section of the superior laryngeal nerves. Laryngeal resistance, measured under constant flow conditions with the larynx removed from the breathing circuit, showed an exaggerated inspiratory decrease during augmented breaths. Passive lung inflations, performed so as to mimic the pattern of augmented breaths, increased dynamic lung compliance but did not elicit changes in EEV or respiratory frequency. The results indicate that the increase in EEV cannot be attributed to increased lung compliance but results from a change in end-expiratory respiratory muscle tone. This change, and the change in respiratory frequency appear to be part of a reflexly evoked central response that includes the augmented breath itself. The larynx participates in the augmented breath, but its mechanical importance is small.     

On the causes of lung hyperinflation during bronchoconstriction

Airway obstruction in asthma and chronic obstructive pulmonary disease (COPD) is often associated with lung hyperinflation. In this review, we examine the mechanisms that may cause functional residual capacity (FRC), residual volume (RV) and total lung capacity (TLC) to increase during acute and chronic airway obstruction. Normally, FRC at rest is determined by the static characteristics of the lung and chest wall. When airways narrow, FRC may be also be determined by dynamic factors. There are data suggesting that expiratory flow limitation during tidal breathing represents the starting trigger for FRC to increase, in order to allow breathing at higher flows. Indeed, the increase in FRC during induced bronchoconstriction in asthma is closely associated with the occurrence of flow limitation, i.e. the achievement of maximum flow during tidal breathing. Conversely, the decrease in FRC following bronchodilatation in COPD is closely associated with flow limitation disappearing or occurring at lower lung volumes. In normal young people, RV is determined by the static characteristics of the chest wall. During bronchoconstriction RV may also be determined by dynamic factors; therefore, changes in flow or airway calibre at low lung volumes may modulate RV during bronchoconstriction. During acutely induced bronchoconstriction, RV achieved with an expiration from TLC is less than with an expiration from tidal breathing, and this effect appears to be linked to the bronchodilator effect of the deep inhalation. The reasons for the increase in TLC during airway narrowing are not clear, but the duration of the bronchoconstriction by itself may play a role.