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.     

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.     

Respiratory effects of cold air breathing in anesthetized cats

Respiratory effects of cold air breathing were studied in anesthetized cats. Two different protocols were used: the air temperature was either lowered in an isolated segment, constituted by the larynx and oropharynx or in lower airways, so that the cats inspired the cold air directly. Temperatures ranged between 37 and 8 degrees C (first protocol) or between 37 and 15 degrees C (second protocol). When the temperature fell below 15 degrees C in the upper segment, marked increase in lung resistance occurred, without any significant changes in ventilatory variables nor in diaphragmatic electrical activity. The section of superior laryngeal nerves abolished this bronchomotor effect. In present experimental circumstances, thermal changes measured in lower airways when cats breathed cold air were mainly located in the cervical trachea. An increase in lung resistance and weak but significant changes in the diaphragmatic electromyogram began when the inspired air temperature fell below 25 degrees C. A selective local block of conduction in small vagal fibres by procaine or section of vagus nerves suppressed all these effects. In all cases the cold-induced changes in lung mechanics began very early (less than 10 sec) but continued for few minutes after the physiological temperature range had been restored in airways. The present data strongly suggest that the bronchomotor response to cold air breathing is a reflex, mediated by afferent fibres in the superior laryngeal nerves and in the vagus nerves.     

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.     

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.     

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 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.     

The respiratory activity of the superior laryngeal nerve in the rat.

The aim of this study was to characterize the laryngeal afferent activity of the rat. The animals were anesthetized and breathing spontaneously. Laryngeal afferent activity was recorded from both the whole superior laryngeal nerve (SLN) and from single fibers isolated from this nerve. An overall inspiratory augmenting activity was observed in the whole SLN during tracheostomy breathing, tracheal occlusion and upper airway breathing, but an expiratory augmenting activity was present during upper airway occlusion. The inspiratory modulated activity was abolished by bilateral section of the hypoglossal nerves but not the recurrent laryngeal nerves. A great number of receptors (46/80, 58%) were identified as 'drive' receptors, and others as 'pressure' (22/80, 28%) and 'irritant' type receptors (9/80, 11%). Nineteen pressure receptors were stimulated by positive transmural pressure, while only three stimulated by negative pressure. Nine drive receptors were also stimulated by positive pressure and inhibited by negative pressure. Such response to pressure was further evaluated by applying maintained pressures to the functionally isolated upper airway. These results are essentially consistent with findings obtained in the rabbit, but differ from those reported for the dog.     

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.     

Breathing pattern in rats with chronic section of the superior laryngeal nerves

In a first set of experiments we registered the integrated afferent activity of the superior laryngeal nerve (SLN) in adult anaesthetized rats. The activity increased with positive upper airway pressure (Pua); with progressively more negative Pua, the SLN activity at first declined then increased again. A second set of adult rats underwent bilateral section of the SLN (SLN denervated) or a sham operation (controls). Both groups appeared to recover promptly from the operation and 6 days later their resting breathing pattern was recorded by the barometric method. SLN denervated rats had a shorter inspiratory time (80%), hence higher frequency and mean inspiratory flow, than controls. During hypoxia (10 min at 10% O2) both groups hyperventilated with an almost identical pattern. The rats were then again anaesthetized and the right vagus cut in an attempt to reduce the afferent component from the lower airways, which may have masked the SLN regulatory contribution. One week after this second operation both SLN denervated and controls breathed more deeply and slowly than before vagotomy, but the pattern was not significantly different between the two groups, either in normoxia or hypoxia. Finally, the rats were anaesthetized and integrated diaphragm activity recorded during spontaneous breathing and the first effort against closure of the nostrils. With both vagi cut, the duration of the occluded effort was slightly longer in SLN denervated than in controls. These results suggest that in adult awake rats laryngeal afferent activity tends to decrease mean inspiratory flow. However, this regulatory contribution is small during eupnea and insignificant during hypoxic hyperventilation.     

Responses of recurrent laryngeal motoneurons to changes of pulmonary afferent inputs

In decerebrate, paralyzed cats ventilated with a cycle-triggered pump, the discharges of the recurrent laryngeal (whole nerve or single fibers) and phrenic nerves, and the changes produced by pulmonary afferent inputs (lung inflation), were compared. When lung inflation was in phase with neural inspiration, four types of laryngeal fiber activities were observed: (a) phasic-inspiratory; (b) tonic-inspiratory; (c) expiratory-inspiratory; (d) early-expiratory. The firing patterns during inspiration were plateau-like, whereas the phrenic pattern was augmenting. When inflation was withheld, the plateau patterns usually became augmenting, indicating inhibition of laryngeal inspiratory activity by pulmonary afferents. Secondary effects of withholding inflation were (a) increases of early-expiratory activity (both whole nerve and individual fiber), indicating increased post-inhibitory rebound excitation; (b) decreased activity of tonic-inspiratory and expiratory-inspiratory fibers during early neural expiration, indicating increased inhibition by early-expiratory neurons. The discharge patterns of different types of laryngeal motoneuron, as well as their changes with inflation, are interpreted in relation to the function of regulating airway resistance.     

Cooling mediates the ventilatory depression associated with airflow through the larynx

Although constant airflow through the upper airway has been shown to induce ventilatory depression in anesthetized newborn animals, the role of laryngeal temperature in this response has not been studied. Experiments were performed in fourteen 1-5 day-old anesthetized puppies breathing through a tracheostomy. Tidal volume and laryngeal temperature were recorded while a constant stream of air (15-25 ml/sec) at room temperature was passed in the expiratory direction for 20 sec through the isolated upper airway. Warm (35-37 degrees C), humidified air at the same flow served as control. When laryngeal temperature was decreased by 7.5 +/- 0.9 degrees C, a marked change in breathing pattern was observed (VT = 54 +/- 5, TI = 187 +/- 33, TE = 636 +/- 179, VT/TI = 45 +/- 10% of control; n = 9). Warm air at the same flow induced no significant changes. Superior laryngeal nerve section abolished the effects of cooling on breathing pattern. In 5 puppies we compared the effect of 'fast' and 'slow' laryngeal cooling. Fast trials altered breathing pattern earlier than slow trials. We conclude that the depressant effect of airflow through the upper airway is entirely due to a decrease in laryngeal temperature and is mediated by superior laryngeal nerve afferents.     

Sulphur dioxide block of laryngeal receptors in rabbits

In 6 rabbits moving average of activity of superior laryngeal nerve(SLN) increased when pressure in upper airways (Pua) was positive and decreased when it was negative. After SO2 exposure of upper airways SLN activity at Pua = 0 decreased to 40% and was no longer affected by changes in Pua. Activity of 67 fibers of SLN was recorded in 11 rabbits: 35 came from 'pressure' receptors, 27 from 'drive', and 5 from 'flow'. Thirty-three pressure receptors discharged at Pua = 0: 32 increased their firing rate with positive Pua and decreased it with negative Pua, one did the reverse. One pressure receptor silent at Pua = 0 fired with positive Pua, the other with negative Pua. Pressure receptors were slowly adapting. SO2 blocked within 3-9 min 84% of pressure receptors, 56% of drive receptors, and 4 out of 5 flow receptors. The receptors recovered control activity within 5-10 min after SO2 removal. SO2 block of laryngeal receptors may represent a convenient experimental tool for studies of laryngeal reflexes.     

Reflex effects on breathing of laryngeal denervation, negative pressure and SO2 in upper airways

Respiratory reflex effects of laryngeal denervation, negative pressure and SO2 in upper airways were studied in anesthetized rabbits. Inspiratory efforts with nasal occlusion had longer duration (TIo) and smaller diaphragm activity (Adi) than with tracheal occlusion. After section of superior laryngeal nerves (SLN) these differences disappeared: values with tracheal occlusion became similar to those with nasal occlusion before denervation. This suggests that laryngeal pressure receptors, firing at zero pressure and decreasing their discharge with negative pressures, increase central inspiratory activity. After SO2 TIo, both with tracheal and nasal occlusion, increased even after laryngeal denervation, provided SO2 flowed through nasal pathway. Hence, nose and/or rhinopharynx contain receptors affected by SO2. After laryngeal denervation and SO2 TIo was shorter with nasal than with tracheal occlusion, despite equal Adi. This, combined with the above findings, suggests two groups of pressure receptors in nose and/or rhinopharynx with opposite effects on inspiratory off-switch: one unaffected and the other probably blocked by SO2. During nose breathing section of SLN produced only a slight decrease in mean inspiratory flow.     

Respiratory heat loss is not the sole stimulus for bronchoconstriction induced by isocapnic hyperpnea with dry air

It is uncertain if respiratory heat loss or respiratory water loss is the stimulus for bronchoconstriction induced by isocapnic hyperpnea or exercise with dry air in subjects with asthma. We partially separated these 2 stimuli by having 18 subjects with asthma breathe dry air (0 mg/L water content) at increasing ventilations by isocapnic hyperpnea while we measured the increase in specific airway resistance (SRaw). The study was divided into 2 phases. In Phase 1, we used an apparatus with a single respiratory valve and evaluated the subjects' responses at 3 different inspired temperatures (-8.4, 20.5, and 39.4 degrees C). Seven of the subjects had esophageal catheters with 2 thermocouples in place to measure retrocardiac and retrotracheal temperatures. In this phase, we found that there were no significant differences in the ventilation required to cause a 100% increase in SRaw among the 3 different inspired temperatures (48.4 L/min, cold; 47.5 L/min, room temperature; 44.2 L/min, hot), even though the retrotracheal temperature fell more when the subjects breathed cold air at 40 L/min (2.1 degrees C) than when they breathed hot air (1.2 degrees C), suggesting greater airway cooling with the cold air. In Phase 2, in order to accurately measure inspired and exhaled temperatures and exhaled water content, we used 2 separate systems for delivering the inspired air and collecting the exhaled air at 2 different inspired temperatures (-21.4 and 38.9 degrees C). Again, we found that there was no significant difference in the ventilation required to cause a 100% increase in SRaw between the 2 different inspired temperatures (28.3 L/min, cold; 33.6 L/min, hot). When the subjects inhaled cold air, exhaled temperature was warmer than previously reported.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of laryngeal anesthesia on pulmonary function testing in normal subjects

Pulmonary function tests (PFT) were performed on 11 normal subjects before and after topical anesthesia of the larynx. The PFT consisted of flow volume loops and body box determinations of functional residual capacity and airway resistance, each performed in triplicate. After the first set of tests, cotton pledgets soaked in 4% lidocaine were held in the pyriform sinuses for 2 min to block the superior laryngeal nerves. In addition, 1.5 ml of 10% cocaine was dropped on the vocal cords via indirect laryngoscopy. PFT were repeated 5 min after anesthesia. Besides routine analysis of the flow volume loops, areas under the inspiratory (Area I) and expiratory (Area E) portions of the loops were calculated by planimetry. Area I, peak inspiratory flow (PIF), as well as forced inspiratory flow at 25, 50, and 75% forced vital capacity (FVC), decreased after anesthesia. Peak expiratory flow decreased after anesthesia, but Area E and forced expiratory flow at 25, 50, and 75% FVC were unchanged. This protocol also was performed in 12 normal subjects with isotonic saline being substituted for the lidocaine and cocaine. In this group, no significant differences were observed when flow volume loop parameters were compared before and after topical application of saline. In 5 spontaneously breathing anesthetized dogs, posterior cricoarytenoid muscle and afferent superior laryngeal nerve activity were recorded before and after laryngeal anesthesia performed with the same procedure used in the human subjects. Laryngeal anesthesia resulted in a substantial decrease or a complete disappearance of afferent SLN activity recorded during unobstructed and obstructed respiration. The data suggest that laryngeal receptors help modulate upper airway patency in man.     

Rhythmic discharge induced by temperature variation and drugs in isolated sympathetic ganglia

Isolated sympathetic ganglia from various mammalian species fire spontaneous, rhythmic discharge when exposed to low temperatures. Extracellular recording from rat, guinea pig, and rabbit superior cervical ganglia as well as dog lumbar ganglion revealed large single potentials or bursts of potentials, occurring at regular intervals, when the bath temperature was kept between 15-30 degrees C. When the temperature was reduced below 15 degrees C or raised above 30 degrees C, the rhythmic discharge decreased in frequency and finally stopped. Rhythmic discharge also appeared when ganglia were treated with emetine or the K(+) channel blockers, cesium and 4-aminopyridine. The frequency and amplitude of potentials and the pattern of rhythm varied from ganglion to ganglion. The single potential or rhythmic burst firing seemed to originate from a single unit or multiple discharging units, as indicated by the amplitude and frequency of the potentials in a burst. The discharge was abolished by ganglionic blocking agents or by the absence of Ca(2+), suggesting a presynaptic origin. The spontaneous rhythmic discharge may be important as a support mechanism for the cardiovascular system in victims of exposure to extreme cold temperature.     

Effect of alpha-adrenergic blockade on exercise-induced asthma and conditioned cold air

Cooling and drying of the intrapulmonary airways have been shown to be important stimuli for the development of bronchospasm induced by exercise and isocapnic cold air hyperventilation. It has also been suggested that alpha-adrenergic receptor activity is increased at lower temperatures. To evaluate the role of alpha-adrenergic activity in the development of bronchoconstriction during airway cooling, we examined the effects of alpha-adrenergic blockade with phentolamine on bronchospasm induced by exercise and isocapnic cold air hyperventilation in 8 asthmatics. Exercise consisted of 6 min of steady-state exercise at 90% predicted maximal heart rate breathing compressed air at 0% humidity and 21 +/- 1 degrees C (mean +/- SD). During baseline exercise studies, FEV1 fell 41.6 +/- 15.8%, but only 12.8 +/- 8.5% during alpha-adrenergic blockade (p less than 0.001). Isocapnic cold air challenge consisted of breathing compressed cold air (0% humidity, -17 +/- 4 degrees C) for 3-min periods, with stepwise increases in minute ventilation (Ve) until the FEV1 fell at least 20%. During baseline cold air challenges, FEV1 fell 20% (PD20 FEV1) at a Ve of 48.8 +/- 21 L/min. However, during alpha-adrenergic blockade 6 asthmatics were able to achieve much higher levels of VE (86.6 +/- 22.7 L/min) before FEV1 fell 20% (p less than 0.01), and 2 asthmatics did not decrease their FEV1 by 20%, despite reaching maximal levels of ventilation of 132 and 108 L/min, respectively. Alpha-adrenergic blockade did not affect airways responses to histamine or ragweed antigen (p greater than 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of airway cooling on tracheal stretch receptors

We studied the effect of cold air on tracheal slowly adapting stretch receptors (SAR) in 6 anesthetized, spontaneously breathing dogs. Air at constant flow and two different temperatures was passed through an isolated segment of the extrathoracic trachea. We recorded SAR action potentials, esophageal pressure, tracheal pressure and temperature. With a reduction in tracheal temperature of approximately 10 degrees C the steady state response of 30 SARs to a distending pressure of 1.0 kPa decreased to 75% of control (P less than 0.001). At lower distending pressure the inhibitory effect of tracheal cooling decreased: 87% of control at 0.5 kPa (P less than 0.05, n = 8) and 96% of control at 0.2 kPa (P greater than 0.05, n = 8). The response of 13 tracheal SARs to sinusoidal pressure oscillations (0.15 kPa) superimposed on a bias pressure (0.5 kPa) was reduced (P less than 0.01) by local cooling to the same extent at the 2 pressure extremes ('peak' value = 71% of control; 'valley' = 67% of control), resulting in a similar change in receptor discharge within the oscillatory cycle. The inhibitory effect of airway cooling on stretch receptors may play a role in cold-induced bronchoconstriction.     

氦-氧混合气治疗哮喘的机理及临床应用探讨

目的探讨氦－氧混合气（Ｈｅｌｉｏｘ，２１％Ｏ２～７９％Ｈｅ）对气道痉挛模型犬及支气管哮喘急性发作患者的作用。方法选择６只健康杂种犬，激发气道痉挛后每次分别吸入Ｈｅｌｉｏｘ和空气（１２ｍｌ／ｋｇ），观察呼吸力学、血液动力学及血气的变化；选择支气管哮喘急性发作患者８例，应用自制的重复利用氦气装置，观察吸入Ｈｅｌｉｏｘ后肺功能、血气的变化。结果Ｈｅｌｉｏｘ可以迅速降低气道压力、气道阻力，降低呼吸功耗，提高肺顺应性；可以促进氧合，提高动脉血氧分压，促进二氧化碳的排除，但后续效应短暂。我们研制的循环式氦－氧混合气辅助呼吸装置可以显著节省氦气消耗，临床应用效果理想。结论Ｈｅｌｉｏｘ可以降低气道压力，促进氧合，促进二氧化碳排除。故而吸入Ｈｅｌｉｏｘ是治疗哮喘的有效手段之一。