Effects of cooling on laryngeal reflexes in the dog

We investigated the reflex effects of laryngeal cooling on posterior cricoarytenoid (PCA) muscle activity, breathing pattern, arterial blood pressure and heart rate. We performed experiments on 9 anesthetized, spontaneously breathing dogs. Laryngeal temperature was decreased by passing cold air through the functionally isolated larynx while the dog was breathing through a tracheostomy. Inspiratory and expiratory durations, esophageal pressure, peak PCA activity, heart rate and blood pressure did not change significantly during laryngeal cooling. Upon interruption of cold airflow, while the laryngeal temperature was returning to control values, we assessed PCA response to upper airway occlusion. At laryngeal temperatures of 20-25 degrees C the peak PCA activity during upper airway occlusion was approximately 2/3 of that observed at control temperature (approximately equal to 33 degrees C). This difference was abolished by topically applied anesthetics or by superior laryngeal nerve section. In addition, we recorded from 4 laryngeal mechanoreceptors stimulated by negative pressure; their response to upper airway occlusion was reduced to 1/2 by laryngeal cooling. These results indicate that laryngeal cooling has a marked depressive effect on the PCA response to collapsing pressure in the larynx, thereby compromising the mechanism subserving upper airway patency.     

Menthol in the upper airway depresses ventilation in newborn dogs.

Upper airway cooling depresses ventilation in the newborn dog. Since airway cooling stimulates laryngeal cold receptors and inhibits laryngeal mechanoreceptors, the type of afferent ending responsible for this reflex cannot be easily identified. l-menthol, a specific stimulant of cold receptors in the absence of any cooling, has been used to ascertain the discrete role of upper airway cold receptors in this ventilatory depression. Experiments were carried out in 8 anesthetized 7-14-day-old dogs breathing through a tracheostomy with the upper airway functionally isolated. Constant flows of warm air (37 degrees C), with and without addition of l-menthol, and cold air (25 degrees C) were delivered through the upper airway in the expiratory direction. As compared to warm air trials, cold air and warm air + l-menthol trials greatly reduced ventilation (57.5 +/- 10.7% and 52.8 +/- 11.7% of control, respectively; P less than 0.01) mostly due to a prolongation of Te (291.2 +/- 106.4% and 339.2 +/- 90.0%, respectively, P less than 0.01). Section of the superior laryngeal nerve abolished the response to cold air. However, a residual depressive effect of l-menthol was still present in 3 of 5 animals and was abolished by nasal anesthesia, suggesting the involvement of nasal cold receptors. The results suggest that in the newborn dog stimulation of laryngeal cold receptors, without any concurrent inhibition of laryngeal mechanoreceptors, is a sufficient stimulus to cause respiratory depression.     

Characteristics of laryngeal cold receptors

This study was designed to further characterize the properties of previously described laryngeal cold receptors (Respir. Physiol. 59:35, 1985). Single unit action potentials were recorded from the internal branch of the superior laryngeal nerve (SLN) in anesthetized, spontaneously breathing dogs. The nervous conduction of fibers originating from 12 laryngeal cold receptors was blocked at a mean (+/- SE) temperature of 18.8 +/- 0.7 degrees C. Twelve receptors were localized on the edge of the vocal folds in correspondence of the vocal process of the arytenoid cartilage. Topical anesthesia (2% lidocaine) blocked their activity within 4-18 sec, suggesting a superficial location. Paralysis of the vocal folds during spontaneous breathing through the upper airway did not alter the activity of 9 of 13 cold receptors. On the other hand, 7 of 12 cold receptors tested with constant flow showed respiratory modulation and laryngeal paralysis abolished the modulation of 3 of these tested with a constant flow of air. During progressive cooling in a stepwise fashion, as in frigid air breathing, laryngeal cold receptors maintained a phasic discharge. Our results indicate that these endings are particularly suited for detecting changes in temperature.     

Effect of cold air on laryngeal mechanoreceptors in the dog

We have previously described laryngeal receptors specifically activated by cooling. The aim of this study is to determine the effect of cold air on laryngeal mechanoreceptors responding primarily to transmural pressure and respiratory movements of the larynx. We have recorded action potentials from 30 single fibers in the peripheral cut end of the internal branch of the superior laryngeal nerve of 11 anesthetized, spontaneously breathing dogs. Of 29 receptors studied with a constant flow of cold air through the isolated upper airway 13 showed a marked reduction in their discharge (0 to 15% of control), 10 showed a moderate decrease (16 to 84% of control) and the remaining 6 were minimally affected. Seven of the 29 receptors showed, prior to the inhibition, a transient initial stimulation. Transient state responses of the most affected receptors lagged behind laryngeal temperature. Three of the most affected endings were also studied during spontaneous breathing of cold air; to a progressive decrease in laryngeal temperature corresponded a progressive decrease in receptor activity. Susceptibility of the receptors to laryngeal cooling and topical anesthesia did not closely correlate. Our results indicate that in evaluating the reflex responses to upper airway cooling both excitation of cold receptors and inhibition of laryngeal mechanoreceptors should be taken into account.     

Laryngeal receptors responding to transmural pressure, airflow and local muscle activity

The larynx has a rich sensory supply which is the main source of several respiratory reflexes. These reflexes, that influence both the patency of the upper airway and the pattern of breathing, are related to transmural pressure and/or airflow in the upper airway. Yet hardly any information is available on the response of laryngeal mechanoreceptors to transmural pressure and airflow. We recorded action potentials from single fibers separated from the superior laryngeal nerve of anesthetized dogs, breathing spontaneously either through a tracheostomy or the upper airway. The airway could be occluded above or below the larynx. On the basis of their behavior during tracheostomy breathing, upper airway breathing, tracheal occlusion and upper airway occlusion, laryngeal mechanoreceptors were classified as pressure receptors, flow receptors or 'drive' receptors (stimulated by the respiratory activity of upper airway muscles). Pressure receptors were encountered most frequently, representing 63.6% of our sample of 110 receptors, 'drive' receptors constituted 21.8% and flow receptors the remaining 14.6%. Our findings indicate that, even though the three types of receptors differ in sensory modality, they concur in exhibiting a predominant activity during inspiration. In fact, 65% of all receptors are active during eupneic inspiration. Moreover, their activity increases markedly during upper airway obstruction.     

Effects of end-expired pressure on phrenic output in servo-ventilated dogs

The pattern of breathing induced by increases in end-expired lung volume (EEVL) was determined in 9 anesthetized dogs. The pulmonary and systemic circulations were separately pump-perfused and the lungs were ventilated with a servo-ventilator actuated from the phrenic neurogram. EEVL was increased as a continuous ramp by slowly raising end-expired transpulmonary pressure from 1.5 to 12 cm H2O. Tidal volume (VT), inspiratory time (TI), and expiratory time (TE) were measured at vagal temperatures of 39 degrees C and 7 degrees C and following vagotomy. At a vagal temperature of 39 degrees C, increasing EEVL produced significant reductions in VT and TI while greatly prolonging TE. Vagal cooling to 7 degrees C, substantially altered the reflex response to increased EEVL. At 7 degrees C, VT decreased as EEVL increased, but the reduction was not so pronounced as at 39 degrees C. In addition, both TI and TE shortened. Increasing EEVL following vagotomy had no consistent effects on breathing pattern. We conclude that increasing EEVL stimulates tachypneic promoting pulmonary afferent nerves, most likely pulmonary C-fibers, but at normal vagal temperature their effect is masked by the stronger reflex inhibition of slowly adapting pulmonary stretch receptors.     

Carbon dioxide-responsive laryngeal receptors in the dog

The purpose of this study was to relate the carbon dioxide (CO2) response of laryngeal receptors to their behavior during the breathing cycle (i.e. their response to transmural pressure changes, laryngeal movement or decreases in temperature) or during exposure to irritant stimuli (water or cigarette smoke). In 9 anesthetized mongrel dogs breathing spontaneously through a tracheostomy, unit activity from the superior laryngeal nerve was recorded while warmed and humidified gas mixtures (air or 10% CO2 in O2) were passed, for 1 min, through the functionally isolated upper airway in the expiratory direction. None of the 10 cold receptors studied were affected by CO2. Eleven of 20 laryngeal non-modulated mechano-receptors were stimulated (from 0.3 to 1.6 imp/sec) by exposure to CO2. These CO2-responsive receptors were also stimulated by known irritant stimuli (cigarette smoke, water), although not all receptors which responded to these irritants were stimulated by CO2. Twelve of 33 respiratory-modulated receptors were affected by CO2; 4 were stimulated and 8 inhibited. Receptors inhibited by CO2 were also inhibited by negative pressure while receptors stimulated by CO2 were also stimulated by negative pressure. These results show that CO2-responsive laryngeal receptors are not specialized endings. Although it is not clear to what extent each separate group of laryngeal receptors is involved, each may contribute to the reflex bradypnea which has been observed during exposure of the upper airway to elevated levels of CO2. However, the importance of CO2-responsive laryngeal receptors in physiological conditions remains unclear.     

Respiratory afferent activity in the superior laryngeal nerves

This study evaluates the afferent activity in the superior laryngeal nerve (SLN) during breathing as well as during occluded inspiratory efforts. Experiments were performed in 11 anesthetized and spontaneously breathing dogs. Electroneurographic activity was recorded from the peripheral cut end of the SLN and, in 3 dogs, also from the contralateral vagus nerve. A tracheal cannula with a side arm allowed the bypass of the larynx during breathing and occluded efforts. A clear inspiratory modulation was present in all experimental conditions. Both peak and duration of the SLN activity decreased (87% and 89%) when breathing was diverted from the upper airway to the tracheostomy. Peak and duration of the SLN activity (as % of upper airway breathing) increased during occluded efforts; however, the increase was greater when the larynx was not by-passed (peak = 118% vs 208%, duration = 143% vs 178%). Section of the ipsilateral recurrent laryngeal nerve reduced the inspiratory modulation. Vagal afferent activity increased equally during tracheostomy and upper airway breathing and decreased markedly during tracheal and upper airway occlusions. Our results indicate that collapsing pressure in the larynx is the major stimulus in activating laryngeal afferents.     

Effect of upper airway negative pressure on respiratory timing

The effects of upper airway negative pressure on respiratory timing and respiratory muscle activity were investigated in 13 urethane-pentobarbital anesthetized adult rabbits. Diaphragm and upper airway muscle EMGs were recorded with fine wire electrodes. The upper airway was converted into a closed system and negative pressure changes were made at will with a syringe attached to a laryngeal cannula. Both inspiratory and expiratory durations (Ti and Te) were prolonged during the negative pressure trials. Maximal prolongation occurred on the first experimental breath for Te and on second breath for Ti. Decreased effects were seen during maintained negative pressures. Peak diaphragm EMG and average slope of diaphragm EMG decreased during these trials. Diaphragmatic apnea (Te greater than or equal to 5 sec) occurred in 15% of trials. In some of these trials apnea lasted as long as the negative pressure stimulus whereas in others spontaneous breathing resumed after a period of apnea. Phasic upper airway muscle activity occurred during diaphragmatic apnea in most of these trials. The superior laryngeal nerve section markedly reduced the effects of negative pressure, indicating that its afferents primarily mediate this response. Our results suggest that upper airway negative pressure acts centrally on both inspiratory and expiratory timing as well as on the motor output of thoracic and upper airway respiratory muscles.     

Nasal 'flow' receptors of the rat

This study was performed to identify trigeminal nasal 'flow' receptors and to investigate their firing characteristics. For this purpose, single unit afferent activity was recorded from the anterior ethmoidal nerve in anesthetized rats breathing through the nose or a tracheostomy. In fourteen rats breathing through the nose, 40 of 73 endings tested were identified as 'flow' receptors for the following characteristics: their spontaneous activity had an inspiratory modulation that disappeared during nasal occlusions, they were markedly stimulated by exposure to cold air and inhibited by warm air. In eleven rats breathing through a tracheostomy, 85 endings were identified as 'flow' receptors being stimulated by a constant nasal airflow (100-300 ml/min) with room air (22-26 degrees C) or cold air (0-15 degrees C), but inhibited with warm air (30-45 degrees C). Fifty-five 'flow' receptors (Type R1 and R2) exhibited a dynamic response to the constant airflow, while the other 30 receptors (Type S) showed a static response. A large proportion of 'flow' receptors (more than 52%) were responsive to tactile stimuli. For all the flow receptors, a decrease in intranasal temperature was the primary factor to excite them. These results suggest that the trigeminal nerve has a number of 'flow' receptors which operate as thermoreceptors.     

Laryngeal afferents activated by phenyldiguanide and their response to cold air or helium-oxygen

In anesthetized cats, sensory neurons in the superior laryngeal nerves (SLN) were identified with respect to their response to (1) phenyldiguanide (PDG) i.v., (2) mechanical stimulation and (3) lowering temperature in an isolated tracheolaryngeal segment. The activity originating from 107 SLN afferent units activated by PDG was recorded using glass microelectrodes advanced in the nodose ganglion. All tested afferent units increased their discharge rate during direct touching of the airway mucosa. None showed flow or pressure related activity during abrupt changes in constant laryngeal flow or transmural pressure in the isolated segment. Fifteen units were inhibited by cold air. Sixty-two units significantly increased their firing rate when the temperature approached 18 degrees C, reached a peak discharge near 15 degrees C, then their activity decreased or stopped. The response to cold air was compared to cold heliox (79% He-21% O2), which enhanced the respiratory heat loss by conduction. The peak firing rate was significantly higher with heliox (+356% compared to +246% with air), the temperature threshold higher (25 degrees C +/- 1.0 degree C) and the temperature range broader (25-11.5 degrees C). Present results show that a large proportion (58%) of afferent SLN fibres activated by PDG are likely non-proprioceptive units, which are stimulated by cooling the inspired gas. Thermosensitive units in the upper airways may act as sensors of the thermal flux through the airway wall more than as detectors of the absolute value of temperature in the airway lumen.     

Reflex bradypnea elicited by cigarette smoke inhaled through an isolated larynx

The respiratory reflex responses elicited by laryngeal exposure to cigarette smoke were studied in 23 chloralose anesthetized dogs. A balloon-in-box system was connected to the breathing circuit, which allowed smoke to be inhaled spontaneously through an isolated larynx while preserving its normal respiratory flow and pressure. Our results in this study showed the following. (1) Two tidal breaths of cigarette smoke inhaled through the larynx triggered a mild but consistent bradypnea: expiratory duration (TE) increased from a control of 3.13 +/- 0.18 sec (mean +/- SEM) to a peak of 4.07 +/- 0.24 sec during smoke inhalation. The slowing of respiration occurred only during the period of smoke inhalation and returned quickly toward control after resuming air breathing. (2) No concomitant cardiovascular response was detected in these animals. (3) There was no significant difference in the prolongation of TE between responses to low- and high-nicotine cigarette smoke. (4) The bradypneic response to smoke was completely abolished by application of topical anesthetic (lidocaine hydrochloride) to the mucosa of this airway segment. These results suggest that the smoke-induced reflex bradypnea is probably elicited by a stimulation of laryngeal afferents.     

Water-responsive laryngeal receptors in the dog are not specialized endings

The primary purpose of this study was to ascertain whether laryngeal receptors activated by water are specialized endings or whether they also respond to other stimuli, such as pressure, temperature and laryngeal motion as they occur during the breathing cycle. In 35 anesthetized mongrel dogs, breathing spontaneously through a lower cervical tracheostomy, water and other test solutions at approximately 37 degrees C were injected into the functionally isolated larynx with a small catheter. Of the 130 receptors studied, none of the cold receptors (N = 13) responded to water, whereas approximately 60% of all laryngeal mechanoreceptors (72 of 117) responded with either a short delay, short duration or a long delay, long duration response. In general the former pattern of response was exhibited by nonrespiratory-modulated receptors, whereas the latter was typical of respiratory-modulated receptors. The specific nature of the stimulus (hypotonicity or lack of chloride ion) of the water response was further studied in 53 receptors with isoosmotic solutions of dextrose and sodium gluconate. The long delay, long duration response was dependent on a decreased osmolality, while the short delay, short duration response was dependent on the lack of chloride ion of the test solutions. All water-responsive receptors tested (N = 17) were blocked within 50 sec by topically applied 2% lidocaine and thus presumed to be superficial. However, 10 receptors which did not respond to water were also blocked within 50 sec, suggesting that not all superficial receptors are stimulated by water. Based on these observations, we propose that changes in osmolality or ionic composition of the laryngeal surface liquid could play an important role in modifying reflexes involved in the maintenance of upper airway patency.     

Effect of upper airway pressure pulses on breathing pattern

Importance of the time of application of upper airway pressure pulses on breathing pattern was investigated in 19 anesthetized, spontaneously breathing rabbits. The upper airway was functionally isolated into a closed system. A servo-respirator, triggered by the inspiratory activity of the diaphragm, was used to apply pressure pulses to the isolated upper airway. Negative pressure pulses of -5, -10, and -15 cm H2O when applied in early inspiration (within the first half) produced a reversible inhibition of inspiration in most trails (86.2%). This resulted in a prolongation of inspiratory duration (TI) and a decrease in mean inspiratory drive (P.Dia/TI) whereas peak diaphragm (P.Dia) activity and expiratory duration (TE) remained largely unaffected. In the remaining 13.8% of trials, an irreversible inhibition with short TI and reduced P.Dia activity was observed. In contrast, with late application of negative pressure pulses the only significant change was a shortening of TI. When positive pressure pulses were applied during expiration, no significant change in TE occurred with either early or late application. A significant prolongation of subsequent TI was seen irrespective of the time of positive pressure application. These results indicate that time of application during the respiratory cycle is an important variable in determining the response to upper airway pressure pulses.     

Alcohol and the response of upper airway resistance to a changing respiratory drive in normal man

We studied the effects of alcohol ingestion on the response of upper airway resistance (UAR) to changing respiratory motor output in 9 normal subjects. Nasal and pharyngeal pressures were measured with two low bias flow catheters placed at the tip of the epiglottis and in the posterior nasopharynx. Respiratory flow was measured with a Fleisch no. 3 pneumotachograph connected to a tightly fitting mask. Breath-by-breath inspiratory upper airway resistances were calculated at isoflow during 1) a CO2 rebreathing (increase in drive), 2) 2 min following five slow vital capacities of 100% O2 (decrease in drive) (Post-O2 period), and 3) 1 min before each procedure (baseline measurements). The respiratory motor output was estimated by the pressure developed 0.1 sec after the onset of inspiration (P0.1) during rebreathing and by the mean inspiratory flow (VT/TI) during the post-O2 period. Measurements were performed before and after the ingestion of 1.5 ml/kg of 40% alcohol. Blood alcohol level rose from 0 to 14.9 +/- 1.8 mmol.L-1 (Mean +/- SD) and total supralaryngeal resistance increased from 2.8 +/- 1.8 cm H2O.L-1.sec to 4.2 +/- 1.8 cm H2O.L-1.sec (P less than 0.001, Student's paired t-test). During CO2 rebreathing UAR decreased exponentially as P0.1 increased both before and after alcohol intake. The slope of the plot Log (pharyngeal resistance) against P0.1 decreased from -17.0 x 10(-3) +/- 9.3 x 10(-3) before alcohol to -11.0 x 10(-3) +/- 6.6 x 10(-3) after alcohol intake (P = 0.03). The slope of the decrease in nasal resistance remained unchanged. A decrease in VT/TI occurred during the Post-O2 period and was accompanied by an exponential increase in UAR at each experiment. The slope of Log (pharyngeal resistance) over VT/TI was significantly higher after (-27.0 x 10(-3) +/- 7.1 x 10(-3)) than before alcohol (-12.0 x 10(-3) +/- 4.2 x 10(-3), P less than 0.001). The slope of the increase in nasal resistance with decreasing VT/TI rose from -8.4 x 10(-3) +/- 6.5 x 10(-3) to -13.0 x 10(-3) +/- 7.4 x 10(-3) after alcohol ingestion (P = 0.06). We conclude that alcohol ingestion depresses the pharyngeal responses to changing central drive in normal subjects.     

Respiratory activity in the superior laryngeal nerve of the rabbit

We studied the respiratory modulation of laryngeal afferents and their response to transmural pressure in 24 anesthetized, spontaneously breathing rabbits. Laryngeal afferent activity has a predominant inspiratory augmentation during tracheal breathing or tracheal occlusion that can be accounted for by the respiratory movement transmitted to the larynx through the trachea. During upper airway breathing or upper airway occlusion SLN afferent activity increases in expiration and decreases in inspiration. This respiratory modulation is due to changes in upper airway pressure (Pua). In fact, positive pressure stimulates SLN afferent activity, while negative pressure inhibits it. Mechanical restriction of epiglottal movement reduced the response to Pua changes during upper airway occlusion and application of maintained positive (0.1-0.5 kPa) and negative (-0.1 to -0.5 kPa) pressures (P less than 0.005). Furthermore, surgical removal of epiglottis decreased the baseline activity of SLN to 16.5% of control. These experiments suggest that in the rabbit the epiglottis is the main source of SLN afferent activity and that its displacement, due to changes in Pua, is the most important factor for modulating SLN activity. Most of the laryngeal receptors showed an inspiratory augmentation with tracheal breathing and occlusion, were stimulated by positive pressure and inhibited by negative pressure, reflecting the behavior observed in the whole nerve.     

Laryngeal pressure receptors

We studied the response characteristics of laryngeal pressure receptors in anesthetized dogs, breathing through a tracheal cannula, by recording single unit action potentials from the peripheral cut end of the internal branch of the superior laryngeal nerve. The larynx, with the rest of the upper airway, was isolated and cannulated separately for the application of distending and collapsing pressures. We identified receptors responding to either negative or positive pressure and a few responding to both. All these receptors showed a marked dynamic sensitivity and had the characteristics of slowly adapting mechanoreceptors. The majority of pressure receptors were active at zero transmural pressure and the gain of their response to pressure was higher at lower values, suggesting a role for these receptors in eupnea. Reflex alterations in breathing pattern and upper airway muscle activity during upper airway pressure changes, previously reported, are presumably mediated by the receptors described here. Moreover, these receptors may play a role in certain pathological states, such as obstructive sleep apnea, in which the upper airway is transiently subjected to large collapsing pressure.     

Ventilation and breathing pattern during progressive hypercapnia and hypoxia after human heart-lung transplantation

The effects of human pulmonary denervation on the ventilatory responses to progressive hyperoxic hypercapnia and isocapnic hypoxia as well as the effect on resting breathing pattern were evaluated in nine female heart-lung transplant (H-LT) recipients. The results were compared to those obtained from 10 normal women of comparable age and stature. Testing was performed 2 to 37 months after H-LT (median, 7.5 months). Cardiac function was normal in all H-LT recipients. None of the patients had spirometric evidence of airway obstruction, while six had a restrictive pattern with forced vital capacities less than 80% of predicted values. Resting minute ventilation (VE), tidal volume (VT), and ventilatory drive (VT/TI) in the H-LT recipients were not significantly different from those of the normal subjects. Inspiratory time (TI), however, was significantly shorter in the H-LT patients (1.64 +/- 0.2 versus 2.09 +/- 0.13 s, p = 0.035), and resting breathing frequency (F) tended to be greater in the H-LT recipients (16.27 +/- 2.04 versus 12.82 +/- 0.53 breaths/min, p = 0.052). The overall ventilatory response to hypercapnia was reduced after H-LT (0.91 +/- 0.17 versus 1.5 +/- 0.27 L/min/mm Hg CO2, p less than 0.043), as was the F response (0.2 +/- 0.09 versus 0.65 +/- 0.13 breaths/min/mm Hg CO2, p less than 0.01). The VT and VT/TI responses to hypercapnia did not differ between the H-LT recipients and normal subjects. There were no significant differences between the two groups with respect to the responses to progressive hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Endogenous opioids modulate the increase in ventilatory output and dyspnea during severe acute bronchoconstriction

The aim of this study was to evaluate whether endogenous opioids are involved in the regulation of breathing pattern and respiratory drive during bronchoconstriction induced by methacholine (MCh). We studied six male asymptomatic asthmatics 18 to 35 yr of age. In a preliminary study we determined the concentration of MCh causing a 60% fall in FEV1 (PC60 FEV1). On two subsequent days, we measured breathing pattern, dyspnea sensation (Borg scale), mouth occlusion pressure (P0.1), and FEV1 before and 10 min after an intravenous injection of either naloxone (0.1 mg/kg) or saline according to a randomized double-blind crossover design. A MCh concentration equal to the PC60 FEV1 was then inhaled, and measurements were repeated 5 min later. Neither placebo nor naloxone affected baseline breathing pattern, P0.1, and FEV1. Naloxone pretreatment did not influence airway response to MCh; the mean percent fall in FEV1 was 65.9 +/- 1.3 and 64.7 +/- 1.2% (mean +/- 1 SE) on the placebo day and the naloxone day, respectively. After MCh inhalation no significant changes in VE, VT, and breathing frequency occurred when patients received placebo. However, P0.1 increased from 1.48 +/- 0.17 to 3.43 +/- 0.70 cm H2O (p less than 0.05), and VT/TI fell from 0.66 +/- 0.08 to 0.52 +/- 0.04 L/s (p less than 0.05). Naloxone pretreatment resulted in an increase in breathing frequency (from 18.2 +/- 1.7 to 22.8 +/- 2.6 breaths/min; p less than 0.05) and VT/TI (from 0.58 +/- 0.06 to 0.74 +/- 0.05 L/s; p less than 0.05) after MCh.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dynamic analysis of airway temperature in dogs breathing cold air]

Exercise in cold, dry air induces bronchoconstriction. However, the time course of airway cooling during the breathing of cold air has not been investigated. In this study in dogs, the temperatures of tracheal gas and the tracheal wall were measured continuously while the animal was breathing cold air at approximately 4.5 degrees C. The temperature of the tracheal gas decreased during the inspiratory phase, increase slightly early in the expiratory phase, and then decreased to the level at end-expiration. The lowest temperature of the tracheal gas decreased significantly, from 29.7 +/- 2.4 degrees C (mean +/- SD) to 25.7 +/- 2.8 degrees C. The highest temperature also changed significantly, but the decrease was less than 1 degree C. The lowest temperature of the tracheal wall decreased from 31.1 +/- 2.6 degrees C to 30.5 +/- 2.5 degrees C during cold-air breathing, but the difference was not significant. When a dog inspired deeply during a cough, the temperature of tracheal gas did not decrease linearly with the progression of inspiration. However, the decrease in the tracheal wall temperature was almost directly proportional to inspiratory volume. We concluded that both the tracheal gas and the tracheal wall temperatures were resistant to cooling with cold-air breathing. It remains uncertain whether rapid, deep breathing during exercise decreased the tracheal wall temperature.