Isocapnic Hyperventilation Research Articles

Hypersensitivity of bronchopulmonary C‐fibers induced by an increase in airway temperature in ovalbumin (Ova)‐sensitized Brown Norway rats.

Our recent study has reported that hyperventilation of humid warm air (WA) triggered cough and reflex bronchoconstriction in patients with mild asthma (AJRCCM 2012). We suggested that sensitization of the bronchopulmonary C‐fibers by increasing airway temperature is involved, but direct evidence is lacking. This study was carried out to determine whether hyperventilation of WA enhanced the pulmonary C‐fiber sensitivity in an animal model of asthma (Ova‐sensitized Brown‐Norway rats). Isocapnic hyperventilation of WA for 3 minutes rapidly raised airway temperature to a peak of ~42°C which significantly elevated the base‐line fiber activity (FA) of pulmonary C‐fibers in Ova rats immediately after the termination of WA challenge, but not in the control rats. Furthermore, the pulmonary C‐fiber response to right atrial injection of capsaicin was significantly higher in Ova rats than control rats before the WA challenge; this difference in the FA response to capsaicin was further amplified after WA in Ova rats (Δ=4.98±1.78 imp/s before, and 10.34±2.21 imp/s after WA; P<0.05, n=9). A similar pattern of the WA‐induced potentiation of the FA response to phenylbiguanide was also founded in Ova rats. These results suggest that Ova‐sensitization increases the excitability of pulmonary C‐fibers, and the hypersensitivity is further enhanced by an increase in the airway temperature. (Supported by NIH and DoD grants)

Bronchial Responsiveness to Dry Air Hyperventilation in Smokers May Predict Decline in Airway Status Using Indirect Methods

BackgroundDisabling respiratory symptoms and rapid decline of lung function may occur in susceptible tobacco smokers. Bronchial hyperresponsiveness (BHR) elicited by direct challenge methods predicts worse lung function outcomes. The aim of this study was to evaluate whether BHR to isocapnic hyperventilation of dry air (IHDA) was associated with rapid deterioration in airway status and respiratory symptoms.MethodsOne hundred twenty-eight smokers and 26 age- and sex-matched healthy individuals with no history of smoking were investigated. All subjects completed a questionnaire. Spirometry and impulse oscillometry (IOS) measurements were recorded before and after 4 min of IHDA. The tests were repeated after 3 years in 102 smokers and 11 controls.ResultsEighty-five smokers (66 %) responded to the challenge with a ≥2.4-Hz increase in resonant frequency (F res), the cutoff limit defining BHR, as recorded by IOS. They had higher F res at baseline compared to nonresponding smokers [12.8 ± 3.2 vs. 11.5 ± 3.4 Hz (p < 0.05)] and lower FEV1 [83 ± 13 vs. 89 ± 13 % predicted (p < 0.05)]. Multivariable logistic regression analysis indicated that wheezing (odds ratio = 3.7, p < 0.01) and coughing (odds ratio = 8.1, p < 0.05) were significantly associated with hyperresponsiveness. An increase in F res was recorded after 3 years in responding smokers but not in nonresponders or controls. The difference remained when subjects with COPD were excluded.ConclusionsThe proportion of hyperresponsive smokers was unexpectedly high and there was a close association between wheezing and coughing and BHR. Only BHR could discriminate smokers with rapid deterioration of airway status from others.

Электрическая активность головного мозга при изокапнической гипервентиляции холодным воздухом

The influence of hyperventilation on electric activity of the brain has traditionally been the subject of study of physiologists. The role of the brain in the processes of adaptation to cold air inhalation is still studied not enough. The aim of the work is to define the peculiarities of brain reaction to isocapnic hyperventilation with cold air and identify correlation between its electric activity against different modes of ventilation and the pattern of breathing and parameters of the forced expiration. 21 healthy volunteers went through complex functional examination. Qualitative differences of relative power of theta rhythm at isocapnic hyperventilation with cold air were found out. The peculiarities of correlation between brain electric activity during cold provocation and breathing pattern and bronchomotor tone were revealed.

Role of β2 Adrenoreceptor Gene Polymorphism in the Formation of Cold Hyperreactivity of the Airways in Asthmatics

The relationship between β(2)-adrenoreceptor gene Arg16Gly polymorphism and bronchial cold reactivity has been studied. Genotype Arg16Arg and allele Arg16 carriership is associated with the development of cold bronchospasm in asthmatics. In addition, a significant reduction of 3,5'-cyclic adenosine monophosphate (cAMP) level has been recorded in Arg16Arg homozygotes on minute 30 after cold provocation in comparison with Gly16Gly genotype carriers. These data indicate the influence of primary dysfunction of β(2)-adrenoreceptors for the formation of bronchial cold hyperreactivity in the patients. Reduced cAMP synthesis by cells in Arg16Arg carriers indicates congenital liability of their β(2)-adrenoreceptors to desensitization during cold air isocapnic hyperventilation test.

Bronchoconstriction Triggered by Breathing Hot Humid Air in Patients with Asthma

Hyperventilation of hot humid air induces transient bronchoconstriction in patients with asthma; the underlying mechanism is not known. Recent studies showed that an increase in temperature activates vagal bronchopulmonary C-fiber sensory nerves, which upon activation can elicit reflex bronchoconstriction. This study was designed to test the hypothesis that the bronchoconstriction induced by increasing airway temperature in patients with asthma is mediated through cholinergic reflex resulting from activation of these airway sensory nerves. Specific airway resistance (SR(aw)) and pulmonary function were measured to determine the airway responses to isocapnic hyperventilation of humidified air at hot (49°C; HA) and room temperature (20-22°C; RA) for 4 minutes in six patients with mild asthma and six healthy subjects. A double-blind design was used to compare the effects between pretreatments with ipratropium bromide and placebo aerosols on the airway responses to HA challenge in these patients. SR(aw) increased by 112% immediately after hyperventilation of HA and by only 38% after RA in patients with asthma. Breathing HA, but not RA, triggered coughs in these patients. In contrast, hyperventilation of HA did not cause cough and increased SR(aw) by only 22% in healthy subjects; there was no difference between their SR(aw) responses to HA and RA challenges. More importantly, pretreatment with ipratropium completely prevented the HA-induced bronchoconstriction in patients with asthma. Bronchoconstriction induced by increasing airway temperature in patients with asthma is mediated through the cholinergic reflex pathway. The concomitant increase in cough response further indicates an involvement of airway sensory nerves, presumably the thermosensitive C-fiber afferents.

Bronchoconstriction induced by hyperventilation with humidified warm air in ovalbumin‐sensitized Brown Norway rats

Previous investigators reported that hyperventilation with hot humid air caused bronchoconstriction in asthmatic patients (Am Rev Resp Dis 131: 357–361, 1985). This study was carried out to further investigate this response in an animal model of allergic asthma. Our results showed: 1) In Brown‐Norway rats actively sensitized by chronic inhalation of ovalbumin (Ova) aerosol, isocapnic hyperventilation with humidified warm air (HWA) for 2 min induced an increase in tracheal temperature (Ttr) to a peak of 40.6 ± 0.3°C and an immediate and sustained (&gt; 10 min) increase in RL (from 0.12 ± 0.01 to 0.21 ± 0.02 cmH2O/ml/s; n=7, P&lt;0.01). In sharp contrast, the HWA challenge produced the same increase in Ttr, but did not generate any increase in RL in matching control rats (n=7, P&gt;0.05). 2) The responses in RL were reproducible in both groups when the same HWA challenge was repeated 60–90 min later (n=4). 3) This bronchoconstrictive effect was temperature dependent; a smaller increase in peak Ttr (39.9 ± 0.2°C) generated a smaller, but significant increase in RL in sensitized rats: from 0.12 ± 0.01 to 0.19 ± 0.03 cmH2O/ml/s (n=3, P&lt;0.05). In conclusion, an increase in airway temperature within the normal physiological range triggered bronchoconstriction in sensitized rats, but not in control rats. Chronic airway inflammation in sensitized animals is likely a major contributing factor in causing this response. (NIH grant HL96914, fellowship NSC98‐2917‐I‐038‐101)

Downregulation of Cough by Exercise and Voluntary Hyperpnea

No information exists on the effects of hyperpnea on the sensory and cognitive aspects of coughing evoked by inhalation of tussigenic agents. The threshold for the cough reflex induced by inhalation of increasing concentrations of ultrasonically nebulized distilled water (fog), and the index of cough reflex sensitivity, was assessed in 12 healthy humans in control conditions, during exercise, and during voluntary isocapnic hyperventilation (VIH) to the same level as the exercise. The intensity of the urge-to-cough (UTC), a cognitive component of coughing, was also recorded throughout the trials. The log-log relationship between inhaled fog concentrations and the correspondingly evoked UTC values, an index of the perceptual magnitude of the UTC sensitivity, was also calculated. Cough appearance was always assessed audiovisually. At an exercise level of 80% of anaerobic threshold, the mean cough threshold was increased from a control value of 1.03 +/- 0.65 to 2.25 +/- 1.14 ml/min (p < 0.01), i.e., cough sensitivity was downregulated. With VIH, the mean (+/-SD) threshold increased from 1.03 +/- 0.65 to 2.42 +/- 1.16 ml/min (p < 0.01), a similar downregulation. With exercise and VIH compared with control, mean UTC values at cough threshold were not significantly changed: control, 3.83 +/- 1.11 cm; exercise, 3.12 +/- 0.82 cm; VIH, 4.08 +/- 1.67 cm. Since the slopes of the log fog concentration/log UTC value were approximately halved during exercise and VIH compared with control, the UTC sensitivity to fog was depressed (p < 0.01). The results indicate that the adjustments brought into action by exercise-induced or voluntary hyperventilation exert inhibitory influences on the sensory and cognitive components of fog-induced cough.

Clinical and functional featuresof respiratory heat exchange and cold airway hyperresponsiveness in patients with bronchial asthma and chronic polypous rhinosinusitis

The aim of the study was to investigate airway conditioning function and cold hyperresponsiveness in patients with bronchial asthma (BA) and nasal polyps. One hundred and eleven asthma patients with or without chronic polypous rhinosinusitis (CPR) were examined. Respiratory heat exchange and cold airway hyperresponsiveness were assessed using thermometry of expired air during quiet breathing and isocapnic hyperventilation with cold air in comparison with a group of healthy persons. The conditioning nasal function was worsened in BA patients with CPRS. Disorders of nasal heat exchange led to decreased temperature of the exhaled air during quiet breathing and cold hyperventilation. These disorders were closely related to increased frequency and severity of cold airway hyperresponsiveness.

Birth weight and adult lung function: a within-pair analysis of twins followed up from birth

The aim of the study was to evaluate whether there is any association between intrauterine growth and later lung function or bronchial reactivity in early adulthood in line with Barker's hypothesis. Nineteen twin pairs with disproportionate intrauterine growth pattern were followed up from birth: either one of the pairs had intrauterine growth retardation (birth weight <2 SD) or the within-pair birth weight difference was >1.3 SD. Flow-volume spirometry, followed by isocapnic hyperventilation of cold air, was performed at the ages of 8-16 and 14-22 years in 1993 and 1999. Wilcoxon's matched-pairs analysis was used to compare smaller and larger twin pairs. In 1993, there were no significant differences between the groups in either spirometry or cold air challenge. In 1999, such a difference was found in forced expiratory volume % (FEV%) and forced expiratory flow (FEF) at 25%-75%, the smaller twin pairs having lower values. In 1993, nine subjects reacted to cold air (>9% decrease in FEV in 1 second). In 1999, only four subjects reacted to cold air, and they all belonged to the group of smaller twins (P=0.04). Lung function evaluated by FEV% and FEF25-75 was lower and responses to cold air were more common at the median age of 16 years in twins with impaired intrauterine growth.

Contrasting effects of isocapnic and hypocapnic hyperventilation on orthostatic circulatory control

The effects of hyperventilation (HV) on mean arterial pressure (MAP) are variable. To identify factors affecting the MAP response to HV, we dissected the effects of hypocapnic HV (HHV) and isocapnic HV (IHV) and evaluated the effects of acute vs. prolonged HHV. In 11 healthy subjects the cardio- and cerebrovascular effects of HHV and IHV vs. normal ventilation were examined for 15 min in the supine position and also for 15 min during 60 degrees head-up tilt. The end-tidal CO(2) of the HHV condition was set at 15-20 mmHg. With HHV in the supine position, mean cerebral blood flow velocity (mCBFV) declined [95% confidence interval (CI) -43 to -34%], heart rate (HR) increased (95% CI 7 to 16 beats/min), but MAP did not change (95% CI -1 to 6 mmHg). However, an augmentation of the supine MAP was observed in the last 10 min of HHV compared with the first 5 min of HHV (95% CI 2 to 12 mmHg). During HHV in the tilted position mCBFV declined (95% CI -28 to -12%) and MAP increased (95% CI 3 to 11 mmHg) without changes in HR. With supine IHV, mCBFV decreased (95% CI -14 to -4%) and MAP increased (95% CI 1 to 13 mmHg) without changes in HR. During IHV in the tilted position MAP was further augmented (95% CI 11 to 20 mmHg) without changes in CBFV or HR. Preventing hypocapnia during HV resulted in a higher MAP, suggesting two contrasting effects of HV on MAP: hypocapnia causing vasodepression and hyperpnea without hypocapnia acting as a vasopressor.

Measurement of Respiratory Muscle Blood Flow in Humans Using Near Infrared Spectroscopy and Indocyanine Green

It has been difficult to measure respiratory muscle blood flow (RMBF) in humans because of the highly invasive measurement techniques and the need to anesthetize patients. To our knowledge, there are no methods available to accurately measure RMBF in conscious humans. PURPOSE: To develop an indicator-dilution approach to measure RMBF using near-infrared spectroscopy (NIRS) to detect indocyanine green dye (ICG) over the respiratory muscles in spontaneously breathing humans. METHODS: NIRS optodes were placed on the left 7th intercostal space at the apposition of the costal diaphragm and on an inactive control muscle (vastus lateralis) in 5 healthy male cyclists. Intravenous injection of ICG allowed cardiac output (by the conventional dye-dilution method with arterial sampling) and RMBF to be measured simultaneously. Esophageal and gastric pressures were also measured to calculate the mechanical work of breathing and trans-diaphragmatic pressure. Measurements were obtained during both resting breathing and three separate 5 minute bouts of constant isocapnic hyperventilation at 27.1±3.2, 56.0±6.1 and 75.9±5.7% of maximum minute ventilation as determined on a previous maximal exercise test. RESULTS: RMBF progressively increased (9.9±0.6, 14.8±2.7, 29.9±5.8 and 50.1±12.5 ml·100ml−1·min) with increasing levels of ventilation while blood flow to the inactive control muscle remained constant (10.39±1.4, 8.7±0.7, 12.9±1.7 and 12.2±1.8 ml·100ml−1·min−1). As ventilation rose, RMBF was closely and significantly correlated with cardiac output (r = 0.994, P = 0.006), the work of breathing (r = 0.995, P= 0.005) and trans-diaphragmatic pressure (r = 0.998, P= 0.002). CONCLUSION: To our knowledge, this is the first study to quantify RMBF in conscious humans during spontaneous hyperventilation. These data suggest that the NIRS-ICG method provides a feasible and sensitive index of respiratory muscle blood flow in humans that should be applicable to rest, light, moderate and heavy exercise.

Exercise-induced depression of the diaphragm motor evoked potential is not affected by non-invasive ventilation

Whole body exercise is followed by a depression of the diaphragm motor evoked potential (MEP). It is unknown whether the change is due to diaphragm activity or whole body exercise. To test the hypothesis that exercise-induced MEP depression was related to diaphragm activity, we performed two experiments. The first examined the effect of whole body exercise, performed with and without the use of non-invasive ventilation (NIV). NIV resulted in significant unloading of the diaphragm (pressure time product 101+/-68 cm H(2)O/s/min versus 278+/-95 cm H(2)O/s/min, p<0.001). Both conditions produced significant MEP depression compared to the control condition (% drop at 5 min, after exercise and exercise with NIV: 29 and 34%, p=0.77). Study 2 compared exercise with isocapnic hyperventilation. At 20 min the MEP had fallen by 29% in the exercise session versus 5% with hyperventilation (p=0.098). We conclude that the work of breathing during whole body exercise is not the primary driver of exercise-induced diaphragm MEP depression.

Expiratory muscles modulate negative expiratory pressure-induced flow during muscular exercise

The recruitment of expiratory muscles during exercise might be altered by the application of negative expiratory pressure (NEP) inducing a feature of expiratory flow limitation (EFL) called muscle EFL. To check this hypothesis EFL and expiratory muscle EMG (ExpEMG) were measured at rest and during exercise in eight healthy subjects. Six subjects performed isocapnic hyperventilation. At 5hPa NEP, 5/8 subjects had EFL during exercise. This limitation disappeared when NEP value was increased and did not appear during isocapnic hyperventilation. During exercise, in limited subjects, ExpEMG was significantly reduced during expiration with NEP as compared to control. Gastric pressure measured in a limited subject increased during expiration but less with NEP than without it, while this pressure measured in another, non-limited, subject decreased. An inhibitory reflex due to negative pressure could be responsible for muscle EFL by reducing expiratory muscle activity. The response to NEP during exercise should be interpreted with caution.

The Effects of Hyperpnea on Exhaled Nitric Oxide Synthesis in Normal Subjects

To determine if the concentration of nitric oxide (NO) in the lungs increases with hyperpnea by contrasting calculated production (ie, the product of the fractional expired NO concentration [FeNO] and minute ventilation [Ve]) [Vno] with the amount of NO in equilibrium with the conducting airways (eNOair) and the amount of NO diffusing from the alveoli (eNOalv). Observational study. University teaching hospital. Normal subjects. Measurements were made in 16 healthy people during and after 4 min of tidal breathing (10 L/min) and isocapnic hyperventilation of 60 L/min. FeNO was measured by collecting the exhaled air during the last minute of each trial and passing it through a chemiluminescence analyzer. The expired NO levels in the plateau phases of slow (30 mL/s) and fast (200 mL/s) single-breath exhalations were also obtained before and after hyperventilation. The Vno (mean +/- SEM) increased from 89.8 +/- 12.3 to 329.1 +/- 36.2 nL/min as Ve rose (p < 0.001). However, neither the quantities of eNOair nor eNOalv changed with hyperventilation (eNOair range before to after, 34.9 +/- 7.7 to 30.9 +/- 6.4 parts per billion [ppb], p = 0.96; eNOalv range before to after, 7.3 +/- 1.5 to 6.5 +/- 1.1 ppb, p = 0.97). These data demonstrate that the amount of NO in equilibrium with the airway walls and alveoli are not altered by hyperpnea. Rather, the apparent augmentation in Vno in such circumstances appears to be an arithmetic artifact.

Bronchial hyper‐responsiveness predicts the development of mild clinical asthma within 2 yr in school children with hay‐fever

In children with mild asthma, symptoms are not always apparent. Therefore, results of tests play an important role for the diagnosis. First, to investigate whether children with bronchial hyper-responsiveness (BHR) but no symptoms of asthma in 1992 had developed clinical asthma at follow up in 1994. The second aim was to find out the diagnostic properties of tests for asthma/allergic inflammation, using either doctor diagnosed asthma (DDA), self-assessed symptoms of asthma or iso-capnic hyperventilation of cold air (IHCA), as the standard, to diagnose asthma in a group of children with hay fever. Twenty-eight children with pollinosis, 12 of them with a history of asthma for the first time during the season 1992, were studied during the birch pollen season and in the autumn of 1994. During both periods, the bronchial hyper-reactivity was estimated by methacholine bronchial provocation tests (MBPT), bronchial variability by peak expiratory flow rate variability, subjective symptoms of asthma by visual analogue scale (VAS) and bronchial inflammation by serum and urine levels of inflammatory mediators. In 1994 IHCA was added during both seasons. Eight of 16 children with BHR but without clinical asthma in 1992 had developed asthma in 1994, 14 of 16 reacted to IHCA and 13 to MBPT. All 12 children with DDA in 1992 had still asthma in 1994 and 14 children with BHR in 1992 had persistent BHR in 1994. Of 23 children with BHR in 1992, 17 had DDA in 1994 and all maintained their BHR. Furthermore, 20 of them reacted to IHCA in 1994. In 1994, 24 of 28 hay-fever children had a positive IHCA tests and 24 had positive MBPT. In relation to VAS, the sensitivity of IHCA and MBPT to predict present asthma was high, but the specificity low, whereas the specificity of most other tests was high, but based on few individuals. In relation to DDA both the IHCA test (65-80%) and the MBPT test (79-85%) had a high sensitivity and it was three to six times more likely to find a positive test among asthmatics than in non-asthmatics. Children with hay fever without clinical asthma have a high risk of developing asthma within 2 yr. In relation to DDA, inhalation of cold air and the MBPT showed a high sensitivity.

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.

Is central nervous system processing altered in patients with heart failure?

Breathlessness is a cardinal symptom of heart failure and the altered regulation of breathing is common. The contribution of abnormal central nervous system activity has not previously been investigated directly, although abnormal autonomic responses have been described. Our aim was to assess whether heart failure patients exhibit different patterns of regional brain activation after exercise stress. We used positron emission tomography with H2(15)O, to measure changes in regional cerebral blood flow (rCBF) and absolute global cerebral blood flow (gCBF) in 6 male class II/III heart failure patients and 6 normal controls. Breathlessness (0-5 visual analogue scale) and respiratory parameters were measured at rest, after horizontal bicycle exercise and during isocapnic hyperventilation. CBF was measured in each condition in all subjects. Both groups were similarly breathless after exercise and the respiratory parameters were comparable. rCBF differences for the main comparison (exercise vs hyperventilation) were: activation of the right frontal medial gyrus (P < 0.001, Z = 4.90) and left precentral gyrus (P < 0.03, Z = 4.66) in controls but not in patients. Both groups had rCBF increases in the left anterior cingulate (P < 0.05, Z = 4.67) and right dorsal cingulate cortex (P < 0.05, Z = 4.66). The gCBF did not differ between exercise, isocapnic hyperventilation and rest in patients but, in controls, gCBF was greater after exercise compared to either isocapnic hyperventilation or rest. Heart failure patients had a distinct pattern of regional cortical activity with exercise-induced breathlessness but unvarying CBF values between conditions. These central neural differences in activity may contribute to some features of heart failure, such as variability in symptoms and autonomic dysregulation.

Single-isomer R-salbutamol is not superior to racemate regarding protection for bronchial hyperresponsiveness

Bronchial hyper-reactivity (BHR) has been suggested to follow cessation of regular medication with racemic salbutamol. This study aimed at investigating the effects from medication with R,S- and R-salbutamol on bronchial response to provocation with isocapnic hyperventilation of cold air (IHCA).Twenty-six patients with mild to moderate asthma were enrolled in a double-blind, randomised, cross-over study. Bronchial response to provocation was measured before and after 1 week's medication. Doses of 0.63mg R-salbutamol or 1.25mg R/S-salbutamol were inhaled three times daily during medication-weeks and a wash-out week intervened. Tests were performed 6h after the last dose of test drug. Impulse oscillometry and forced expiratory volume during one second were methods used to identify bronchial response to provocation. Two patients withdrew from the investigation due to side-effects, one from R- the other from R,S-salbutamol.Comparable resting bronchial conditions were indicated by differences in baseline lung function values of <2% between study days. No statistically significant medication-dependent differences in BHR could be demonstrated between treatment groups. However, 15 patients exhibited higher (P=0.03) post-treatment BHR after pure R-salbutamol than after R,S-salbutamol. Furthermore, plasma concentrations of R-salbutamol tended to be lower (P=0.08) after medication with R- than after R,S-salbutamol despite equal doses of R-salbutamol given during the two separate treatment periods. We also found that considerable amounts of S-salbutamol were retrieved in plasma after medication with pure R-salbutamol.We conclude that we were unable to demonstrate favourable effects of R-salbutamol over R,S-salbutamol regarding response to provocation with IHCA after regular medication of 1 week's duration.

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.

Laser acupuncture in children and adolescents with exercise induced asthma

Background: Laser acupuncture, a painless technique, is a widely used alternative treatment method for childhood asthma, although its efficacy has not been proved in controlled clinical studies. Methods: A double...