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At least 217 records · Page 12Linked to original sources
PubMed1987

Indirect assessment of mucosal surface temperatures in the airways: theory and tests.

We developed and tested a method, based on conduction heat transfer analysis, to infer airway mucosal temperatures from airstream temperature-time profiles during breath-hold maneuvers. The method assumes that radial conduction of heat from the mucosal wall to inspired air dominates heat exchange during a breath-hold maneuver and uses a simplified conservation of energy analysis to extrapolate wall temperatures from air temperature vs. time profiles. Validation studies were performed by simultaneously measuring air and wall temperatures by use of a retractable basket probe in the upper airways of human volunteers and intrathoracic airways of paralyzed intubated dogs during breath holding. In both protocols, a good correlation was demonstrated between directly measured wall temperatures and those calculated from adjacent airstream temperature vs. time profiles during a breath hold. We then calculated intrathoracic bronchial wall temperatures from breath-hold airstream temperature-time profiles recorded in normal human subjects after cold air hyperpnea at 30 and 80 l/min. The calculations show airway wall temperatures in the upper intrathoracic airways that are below core body temperature during hyperpnea of frigid air and upper thoracic airways that are cooler than more peripheral airways. The data suggest that the magnitude of local intrathoracic heat/water flux is not represented by heat/water loss measurements at the airway opening. Both the magnitude and locus of heat transport during cold gas hyperventilation vary with changes in inspired gas temperature and minute ventilation; both may be important determinants of airway responses.

Animals↗
PubMed1989

Longitudinal distribution of canine respiratory heat and water exchanges.

We assessed the longitudinal distribution of intra-airway heat and water exchanges and their effects on airway wall temperature by directly measuring respiratory fluctuations in airstream temperature and humidity, as well as airway wall temperature, at multiple sites along the airways of endotracheally intubated dogs. By comparing these axial thermal and water profiles, we have demonstrated that increasing minute ventilation of cold or warm dry air leads to 1) further penetration of unconditioned air into the lung, 2) a shift of the principal site of total respiratory heat loss from the trachea to the bronchi, and 3) alteration of the relative contributions of conductive and evaporative heat losses to local total (conductive plus evaporative) heat loss. These changes were not accurately reflected in global measurements of respiratory heat and water exchange made at the free end of the endotracheal tube. Raising the temperature of inspired dry air from frigid to near body temperature principally altered the mechanism of airway cooling but did not influence airway mucosal temperature substantially. When local heat loss was increased from both trachea and bronchi (by increasing minute ventilation), only the tracheal mucosal temperature fell appreciably (up to 4.0 degrees C), even though the rise in heat loss from the bronchi about doubled that in the trachea. Thus it appears that the bronchi are better able to resist changes in airway wall temperature than is the trachea. These data indicate that the sites, magnitudes, and mechanisms of respiratory heat loss vary appreciably with breathing pattern and inspired gas temperature and that these changes cannot be predicted from measurements made at the mouth. In addition, they demonstrate that local heat (and presumably, water) sources that replenish mucosal heat and water lost to the airstream are important in determining the degree of local airway cooling (and presumably, drying).

Animals↗
PubMed1994

Inhaled furosemide attenuates hyperpnea-induced obstruction and intra-airway thermal gradients.

Inhaled furosemide attenuates exercise- and isocapnic hyperventilation-induced asthma; however, the mechanism for this phenomenon is unknown. Because the magnitude of the intra-airway thermal gradient that develops between the cooling of hyperpnea and the rewarming that occurs once hyperventilation ceases is directly related to the severity of thermally induced obstruction in humans, we wondered if furosemide blunted these temperature changes. To explore this issue, eight asthmatic subjects had tracheobronchial airstream temperature measures as they performed isocapnic hyperventilation with frigid air alone (HV) or with pretreatment with inhaled saline (S + HV) or 45 +/- 3 (SE) mg of furosemide (F + HV). HV and S + HV resulted in similar degrees of obstruction, whereas the mechanical decrements after F + HV were significantly less. In concert with this protective effect, F + HV resulted in less airstream cooling during hyperventilation and slower rewarming in the recovery period. Because the major source of heat to the airways is provided by its microcirculation, inhaled furosemide may be acting as a topical vasodilator serving to enhance heat availability and thus reducing the effective thermal burden of hyperpnea.

Administration, Inhalation↗
PubMed1994

Relationship between Cr and breathing pattern in mechanically ventilated patients.

In mechanically ventilated patients the natural gas-conditioning process of the upper airways is bypassed by the use of an endotracheal tube or a tracheostomy. We hypothesized that under these conditions the breathing pattern may greatly influence the convective respiratory heat loss (Cr). Cr values were computed from minute ventilation (VE) and inspiratory and expiratory gas temperatures, which were measured in six patients under mechanical ventilation for the management of cranial trauma. In each patient the effects of 11-20 different breathing patterns were investigated. Relationships between Cr and VE and between combined tidal volume and respiratory frequency were obtained by simple and multiple linear regression methods, respectively. Comparison of the standard errors of estimate indicated that multiple linear regression gives the best fit. Thus, Cr was highly dependent on the breathing pattern and was not related only to VE. For the same VE value, Cr was higher when VE was achieved with high tidal volume and low respiratory frequency. These data are consistent with previous studies in which thermal exchanges through the upper airways were taxed by hyperventilation of frigid air.

Adult↗
PubMed2001

Inhibition of nitric oxide synthesis attenuates thermally induced asthma.

To determine whether the inhibition of nitric oxide (NO) synthesis attenuates thermally induced obstruction, we had 10 asthmatic volunteers perform isocapnic hyperventilation with frigid air after inhaling 1 mg of N(G)-monomethyl-L-arginine (L-NMMA) or isotonic saline in a blinded fashion. The challenges were identical in all respects, and there were no differences in baseline lung function [1-s forced expiratory volume (FEV(1)); saline 2.8 +/- 0.3 liters, L-NMMA 2.9 +/- 0.3 liters; P = 0.41] or prechallenge fractional concentration of nitric oxide in the exhaled air (FENO) [saline 23 +/- 6 parts/billion (ppb), L-NMMA 18 +/- 4 ppb; P = 0.51]. Neither treatment had any impact on the FEV(1), pulse, or blood pressure. After L-NMMA, FENO fell significantly (P < 0.0001), the stimulus-response curves shifted to the right, and the minute ventilation required to reduce the FEV(1) 20% rose 53.5% over control (P = 0.02). The results of this study demonstrate that NO generated from the airways of asthmatic individuals may play an important role in the pathogenesis of thermally induced asthma.

Administration, Inhalation↗
PubMed2002

Desiccation and hypertonicity of the airway surface fluid and thermally induced asthma.

To determine whether drying and hypertonicity of the airway surface fluid (ASF) are involved in thermally induced asthma, nine subjects performed isocapnic hyperventilation (HV) (minute ventilation 62.2 +/- 8.3 l/min) of frigid air (-8.9 +/- 3.3 degrees C) while periciliary fluid was collected endoscopically from the trachea. Osmolality was measured by freezing-point depression. The baseline 1-s forced expiratory volume was 73 +/- 4% of predicted and fell 26.4% 10 min postchallenge (P > 0.0001). The volume of ASF collected was 11.0 +/- 2.2 microl at rest and remained constant during and after HV as the airways narrowed (HV 10.6 +/- 1.9, recovery 6.5 +/- 1.7 microl; P = 0.18). The osmolality also remained stable throughout (rest 336 +/- 16, HV 339 +/- 16, and recovery 352 +/- 19 mosmol/kgH(2)O, P = 0.76). These data demonstrate that airway desiccation and hypertonicity of the ASF do not develop during hyperpnea in asthma; therefore, other mechanisms must cause exercise- and hyperventilation-induced airflow limitation.

Adult↗
PubMed2002

Influence of hyperpnea on airway surface fluid volume and osmolarity in normal humans.

To determine the effect of hyperpnea on the characteristics of periciliary liquid, we collected airway surface fluid (ASF) and measured its osmolarity in 11 normal people while they breathed dry, frigid air (-17 +/- 1.2 degrees C) at minute ventilations (VE) of 10, 40, and 80 l/min through a heat exchanger. The ASF was collected at the fifth tracheal ring by absorption onto filter paper pledgets inserted via fiber-optic bronchoscopy. Hyperpnea had no influence on the amount of ASF recovered (ASF volume at a VE of 10 l/min = 12.0 +/- 2.0 microl; at 80 l/min = 8.8 +/- 1.5 microl; P = 0.28) or its osmolarity (at a VE of 10, 40, and 80 l/min = 326 +/- 15, 323 +/- 11, and 337 +/- 12 mosM, respectively; P = 0.65). These findings demonstrate that the tracheal mucosa of normal subjects does not dessicate during hyperpnea and that hypertonicity of the periciliary fluid does not develop even at high levels of ventilation.

Adult↗
PubMed2004

Morphometric changes after thermal and methacholine bronchoprovocations.

To determine whether there are distinctions in the location and pattern of response between different bronchoprovocations, we performed high-resolution computer-assisted tomography in 10 asthmatic subjects before and after isocapnic hyperventilation of frigid air (HV) and methacholine (Meth). The luminal areas of the trachea, main stem, lobar, and segmental bronchi were computed before and after each provocation and blindly compared. Both stimuli reduced the 1-s forced expiratory volume similarly (percent change in 1-s forced expiratory volume HV = 28.1 +/- 5.5%, Meth = 25.8 +/- 5.2%; P = 0.69) but did so in different fashions. Each provocation was associated with the development of both bronchial narrowing and dilation; however, more airways constricted with HV (67.7%) than with Meth (47.0%; P < 0.001). Furthermore, there was little concordance between either the magnitude or direction of change between stimuli in any region of the lung (r = 0.25). In general, the frequency of narrowing increased with branching. Constriction became more prominent in the lobar regions and increased further in the segmental branches, but a wide range of intensity existed. These data demonstrate that provocational stimuli evoke complex morphometric changes within the tracheobronchial tree and that different agonists produce different patterns. Thermal stimuli chiefly influence the segmental level, whereas the response to Meth develops more distally. Even within this distribution, the same airway does not respond in an identical fashion to different stimuli, so there does not appear to be a uniform trigger zone.

Adult↗
PubMed1996

Vocal cord dysfunction masquerading as exercise-induced asthma. a physiologic cause for "choking" during athletic activities.

Exercise-induced bronchospasm is a common clinical problem that is particularly troubling for patients who engage in strenuous physical activity, such as athletes. When such individuals develop this condition, the associated airway narrowing can materially interfere with performance; however, events other than asthma can also produce these symptoms and their differentiation is essential for proper treatment. The present report describes seven elite athletes with psychogenic vocal cord dysfunction who presented with acute dyspnea during sporting competitions. Although the combination of exertion and wheezing suggested the diagnosis of exercise-induced asthma, the patients' histories were sufficiently unique so as to represent a recognizable syndrome. The patients underwent clinical physiologic evaluations including bronchoprovocations with isocapnic hyperventilation of frigid air, methacholine and/or exercise. Direct laryngoscopy was also performed in some subjects. The findings that differentiated these patients from asthmatics were a lack of consistency in the development of symptoms when exposed to identical stimuli, the onset of breathing difficulties during exercise, and poor therapeutic and prophylactic responses to anti-asthma medications. The clinical impression of a functional disorder was confirmed by bronchoprovocations that demonstrated the variable extrathoracic airway obstruction of vocal cord dysfunction. Patients with atypical exertional complaints require careful clinical and physiologic evaluation. The mere association of exercise and airway obstruction is not sufficient to establish the diagnosis of asthma.

Adolescent↗
PubMed1999

Thermally induced asthma and airway drying.

The purpose of this study was to determine whether mucosal dehydration causes thermally induced asthma. To provide data on this point, we studied the effects on lung function of progressive water loss (WL) from the respiratory tract by having eight subjects perform isocapnic hyperventilation for 1, 2, 4, and 8 min at a constant level (V E = 57.5 +/- 6.3 L/min [mean +/- SEM]) while they breathed dry air at frigid (TI = -12.5 +/- 2.7 degrees C) (cold trial) and ambient (24.3 +/- 0.7 degrees C) (warm trial) temperatures. Expired temperatures (TE) were continuously monitored, and WL from the intrathoracic airways was calculated from published relationships. FEV1 was measured before and after each challenge. Each inspirate produced stimulus-response decrements in FEV1, but the effect of cold air was greater (% Delta cold8min = 30.0 +/- 4.7%, warm = 16.0 +/- 4.4%; p = 0.01). Water loss, however, was significantly less in the cold experiment because TE was lower (WL cold8min = 4.8 +/- 0.4 g, warm = 7.1 +/- 0.7 g; p = 0.001; TE cold8min = 22.8 +/- 2.3 degrees C, warm 30.9 +/- 1.5 degrees C; p = 0.003). The FEV1 decreased as WL rose, but the largest intrathoracic losses were associated with the smallest obstructive response (% DeltaFEV1 cold8min = 30%, WL = 4.7 mg; % DeltaFEV1 warm8min = 16%, WL = 7.1 mg; p = 0.002). These data show that removal of water from the lower respiratory tract, and by inference the development of a hyperosmolar periciliary fluid, do not appear to be the primary causes of thermally induced asthma.

Adult↗
PubMed2001

Exhaled nitric oxide and thermally induced asthma.

The purpose of the present study was to determine if nitric oxide (NO) is involved in the pathogenesis of thermally induced asthma. To provide data on this issue, 10 normal and 13 asthmatic subjects performed isocapnic hyperventilation with frigid air while the fractional concentration of NO in the expirate air (FENO) was serially monitored with a chemiluminescence analyzer. FEV1 was measured before and after hyperpnea. Prior to and throughout the challenge, the asthmatics had significantly larger values for FENO (baseline FENO normal, 11 +/- 2 ppb; asthma, 16 +/- 1; p = 0.03). Posthyperpnea, the normal subjects had little change in bronchial caliber (deltaFEV1 baseline to 5 min posthyperpnea, -3.5 +/- 1.5%; p = 0.06), whereas the patients with asthma developed significant airway obstruction (deltaFEV1, -27.7 +/- 2.9%; p = 0.0001). During hyperventilation, the volume of NO rose in both groups. The asthmatic subjects, however, generated approximately 55% more NO/min than did the normal control subjects even though their level of ventilation was approximately 66% less. In contrast to the normal subjects, NO production in the asthmatics continued into the recovery period after the challenge stopped and FENO rose temporally as the airflow limitation developed. These results suggest that NO plays an intimate role in the development of airway obstruction that follows hyperpnea.

Adult↗
PubMed1988

Re-examination of the late asthmatic response to exercise.

To determine the nature of the delayed response to exercise, we had 20 atopic asthmatics perform cycle ergometry on 2 occasions while breathing either frigid or hot-humid air in a random fashion. The latter served as a sham control. Forced expiratory volume in one second (FEV1) was measured serially for 10 h after each trial. Subjects developing a second wave of obstruction after recovery from the initial asthma attack were rechallenged on a third day with methacholine and followed in an identical fashion. Cold-air exercise produced an immediate 28% fall in FEV1 for the group as a whole, after which 2 distinct patterns of recovery developed. In 13 subjects, the initial obstruction resolved over several hours. Thereafter, lung function remained constant. In the remaining 7 subjects, the early attack was followed by an initial improvement and then progressive deterioration. This pattern occurred at the same times and to the same magnitude both in the hot-humid experiment in which the initial obstruction was absent, and when the obstruction was induced with methacholine. Based on these observations, it appears that the late asthmatic reaction that follows physical exertion in some subjects is a nonspecific epiphenomenon that is neither dependent upon the existence of an early response nor is unique to exercise.

Adult↗
PubMed1988

Comparison of intraairway temperatures in normal and asthmatic subjects after hyperpnea with hot, cold, and ambient air.

To determine how the inhalation of hot dry, frigid, and room temperature air influences airway heat transfers, we obtained single-breath temperature washout curves in eight asthmatic and eight normal subjects before and during periods of hyperpnea. The order of study was randomly determined, and the thermal events with each inspirate were correlated with their effects on lung function. Each inspired air condition produced significant airway cooling in both groups. Cold air evoked the greatest response, followed thereafter by hot dry and then room air. Only the asthmatic subjects developed airway obstruction. These data demonstrate that hot dry gases facilitate evaporative cooling and do not keep the airways warm as has been previously suggested. It appears the airway cooling is a normal part of respiration and develops whenever air is inhaled that requires the transfer of heat and/or water to bring the inspirate to body conditions.

Adult↗
PubMed1980

The effects of cromolyn sodium on the airway response to hyperpnea and cold air in asthma.

In order to determine if cromolyn sodium provided protection against the marked bronchoconstriction that develops when the hyperpnea of exercise is combined with frigid air, we exposed a group of asymptomatic asthmatics to this stimulus, with and without pretreatment with this drug. Respiratory heat loss and retrotracheal and retrocardiac esophageal temperatures were measured during each challenge, and multiple aspects of pulmonary mechanics were recorded before commencement and after completion. The results demonstrated that, unlike anticholinergic agents, cromolyn sodium attenuates the obstructive response observed with these large thermal burdens, and does so without affecting airway cooling.

Adult↗
PubMed1984

Influence of cromolyn sodium on airway temperature in normal subjects.

It is well established that cromolyn sodium attenuates the bronchoconstriction induced by airway cooling in both normal and asthmatic subjects. To determine whether this protection derives from a modification of the thermal events that transpire during the conditioning of inspired air, we first recorded the effect of cromolyn on the bronchoconstrictor response to hyperventilation with frigid air in 7 normal subjects. On a separate occasion, we imposed the same thermal burden and measured the temperature at multiple sites within the airways before and after pretreatment with cromolyn. The first cold air challenge produced a significant decrease in forced expiratory volume in one second (FEV1) of 5.5 +/- 0.9% (SEM) and these changes were significantly reduced by cromolyn (FEV1 = 2.8 +/- 0.9%; p less than 0.05). In concert with the improvement in mechanics, the temperatures (T) within the trachea (tr) and the anterior segment of the right lower lobe (AS-RLL) were significantly higher after cromolyn (Ttr = 1.3 +/- 0.2 degrees C; p less than 0.01; TAS-RLL = 1.0 +/- 0.4 degrees C; p = 0.05), and there was a direct positive relationship between the mechanical protection offered by the drug and the increase in airway temperature (Spearman's rank correlation coefficient = 0.83; p = 0.05). These data suggest that cromolyn modifies respiratory heat exchange in such a fashion as to limit airway cooling. The mechanism of this action is not presently known but may reflect a direct or indirect influence on the bronchial vasculature.

Adult↗
PubMed1985

Breathing pattern affects airway wall temperature during cold air hyperpnea in humans.

We studied the influence of flow rate on respiratory heat exchange in 9 healthy adult subjects using a new noninvasive technique, the single-breath temperature washout (SBTW) curve. The SBTW curve is a plot of exhaled gas temperature versus exhaled volume during a standard exhalation and consists of an initial rise (within the first 200 ml) to a plateau temperature that persists through the remainder of exhalation. We found that exhaled gas temperatures within the initial expirate were colder at every airway locus than corresponding intra-airway gas temperatures at end-inspiration, suggesting that heat exchange occurs between lumenal gas and the relatively cooler airway walls during exhalation. The SBTW plateau temperatures were: (1) lower after preconditioning the airways with rapid (80 L/min) isocapnic hyperpnea of frigid air than after less rapid (40 L/min) cold-air hyperpnea or after quiet breathing; (2) lower when, after identical airway preconditioning regimens, the SBTW exhalation was performed with a slower (0.5 versus 2.5 L/s) expiratory flow; and (3) lower when SBTW curves were obtained after airway preconditioning using respiratory patterns with larger inspiration-expiration duration (I:E) ratios (5:1 versus 1:5) at fixed minute ventilation and respiratory rate. Our results indicate that the global respiratory gas-wall heat transfer coefficient increases with velocity to the 0.9 power, a finding similar to that in previous studies of turbulent flow in rigid pipes.

Adult↗
PubMed1982

Direct recordings of the temperatures in the tracheobronchial tree in normal man.

In an effect to determine how far inspired air could penetrate into the respiratory tract before being brought to body conditions, we measured the temperature in the airways of the anterior basilar segment of the right lower lobe in five normal subjects while they breathed air at subfreezing and ambient conditions. During quiet breathing, most of the heating of the incoming gas took place in the upper airways as expected. However, as the thermal burden was increased by rapid inspirations, frigid air, and hyperventilation, the temperature of the distal airways progressively fell and the point at which the incoming air reached body conditions moved deep into the periphery of the lung. These findings demonstrate that heat and water transfer is not localized to one region, but rather is a continuous process that begins the moment the air enters the body and involves as much of the respiratory tract as necessary to complete the task.

Adult↗
PubMed1985

Intraairway thermal profiles during exercise and hyperventilation in normal man.

When large volumes of air are inhaled at rapid rates of ventilation, substantial segments of the tracheobronchial tree become involved in the conditioning process and the inspirate does not reach body conditions of temperature and humidity until it passes well into the peripheral bronchi. To determine if the manner in which ventilation is elevated is an important factor in producing this response, we measured the temperature of the airstream at six points in the tracheobronchial tree from the pharynx to the subsegmental bronchi during 5 min of exercise and voluntary hyperventilation in seven normal subjects while they inhaled frigid air. Minute ventilation and respiratory frequency were recorded at minute intervals and intrathoracic temperatures were measured continuously. With both forms of hyperpnea, airway temperature fell dramatically, and there were no significant differences between exercise and hyperventilation. These results demonstrate that the thermal events that occur within the lung during short, moderately intense degrees of exercise can be readily simulated by voluntary hyperventilation when ventilation and inspired air conditions are matched. Our data also indicate that this form of exercise does not result in an increase in airstream temperature and raise the possibility that the bronchial blood supply may be determined by the local thermal needs of the airways to recover heat and water independent of, at least moderate, increases in cardiac output.

Adult↗