Changes In Airway Caliber Research Articles

Influence of airway calibre on the intrapulmonary dose and distribution of inhaled aerosol in normal and asthmatic subjects

We investigated the relationship between airway calibre and the dose and distribution of inhaled aerosol in ten normal and six asthmatic subjects. Subjects inhaled saline aerosol containing 99mTcO4 delivered from a nebulizer connected to a dosimeter, and the lung fields were scanned with a gamma-camera. Right lung dose (RLD) was calculated as percentage of total dose. Intrapulmonary distribution was measured as penetration index (PI) (peripheral zone counts/central zone counts). Asthmatics had a significantly lower PI than normal subjects and there was a linear relationship between PI and baseline specific airway conductance (sGaw, p less than 0.001), and forced expiratory volume in one second (FEV1, p less than 0.05). After bronchodilatation with salbutamol (delta sGaw 101 +/- 31%, mean +/- SEM), PI increased from 0.73 +/- 0.11 to 1.09 +/- 0.15 (p less than 0.05); after bronchoconstriction with methacholine (delta sGaw 62.6 +/- 2.9%), PI decreased from 1.42 +/- 0.24 to 1.06 +/- 0.22 (p less than 0.05). Changes of PI were correlated with changes in sGaw and FEV1 (n = 20, p less than 0.001) but changes of RLD and changes in airway calibre were not. The distribution of inhaled aerosol, but not the dose, is largely dependent on airway calibre. The differences in PI between normal and asthmatic subjects may at best be explained by the differences in central airway calibre.

Increases in airway responsiveness to histamine precede allergen-induced late asthmatic responses

Changes in airway responsiveness to histamine after allergen inhalation challenge were studied in 14 nonsmoking atopic adult subjects with asthma. Inhalation challenges with allergen and with phosphate-buffered saline (control challenge) were performed single blind in random order, with an interval of 14 days. The development of a late asthmatic response was accompanied by an increase in airway histamine responsiveness that was significant when it was compared with the airway histamine responsiveness after the control challenge at 3 hours ( p < 0.01), 24 hours ( p < 0.01), and 48 hours ( p < 0.02), with recovery at 2 weeks after allergen inhalation. The 3-hour changes in airway responsiveness occurred independently of changes in airway caliber and correlated with the magnitude of the subsequent late response ( r = 0.86; p < 0.001). These results suggest that the tissue events (possibly airway inflammation) that underlie the late asthmatic response may occur before this response becomes clinically apparent.

Effect of salbutamol and inhaled sodium cromoglycate on the airway and neutrophil chemotactic activity in “fog”-induced bronchospasm

To investigate whether salbutamol and sodium cromoglycate (SCG) inhibit airway response and the associated mediator release induced by ultrasonic nebulation of distilled water (UNDW, “fog”), we measured the serum neutrophil chemotactic activity (NCA) during bronchial challenge with “fog” with and without premedication with placebo, salbutamol, or SCG in 10 subjects with asthma, in four sets of studies. To assess changes in airway caliber, we measured FEV 1. To assess changes in NCA, we measured the maximal distance reached by neutrophils in a filter when neutrophils were challenged with the subject's serum in a Boyden chamber. Treatment with placebo did not change baseline FEV 1 or serum NCA; however, FEV 1 decreased and serum NCA increased ( p < 0.05) after inhalation of “fog.” Treatment with SCG did not affect either FEV 1 and baseline serum NCA. After inhalation of “fog,” no significant bronchoconstriction nor NCA increase was observed in eight of 10 patients with maximal mean percent decrease in FEV 1 of −4.26, SEM 0.99, and maximal mean percent increase in NCA of +8.6, SEM 5.28. In the two patients who developed a bronchoconstriction after challenge with SCG pretreatment, an associated significant increase in NCA was observed but did not affect baseline NCA. After inhalation of “fog,” no significant decrease in FEV 1 (maximal mean percent decrease FEV 1, −6.71, SEM 0.17) nor significant increase in serum NCA (maximal mean percent increase NCA, +3.6, SEM 7.1) was observed in nine of 10 patients. After salbutamol, only one patient developed a bronchoconstrictive response to “fog” associated with a significant increase in serum NCA. These results suggest that both SCG and salbutamol may prevent the bronchoconstriction induced by “fog” by inhibiting mediator release.

Lung inflation does not increase maximal expiratory flow during induced obstruction in the dog.

A deep inflation (DI) reverses induced bronchoconstriction in normal human subjects whether assessed by airway resistance before and after a DI or by isovolumic maximal expiratory flows (Vmax) from partial expiratory flow-volume (PEFV) vs. maximum expiratory flow-volume (MEFV) maneuvers. These observations suggest that with induced constriction the hysteresis of airways exceeds that of the parenchyma. In contrast with humans, a previous study of ours on dogs indicated that induced increases in airway resistance were unaffected by DI, suggesting that hysteresis of airways and parenchyma were equal. We hypothesized therefore that in constricted dog lungs, any differences that might arise in isovolumic Vmax between PEFV and MEFV maneuvers would not be due to changes in airway caliber but rather would be wholly determined by isovolumic differences in deflational recoil pressures. Recoil pressures were dynamically measured using six separate alveolar capsules in each of six dogs. At base line there were no significant differences between isovolumic recoil pressures or maximal flows with volume history, suggesting equal degrees of airway and parenchymal hysteresis. After histamine-induced constriction there were also no isovolumic differences in flows, but due to striking nonhomogeneities in dynamic recoil pressure among alveolar capsules, it was not possible to express a single meaningful recoil pressure pertinent to the lungs as a whole. These findings are consistent with the idea that isovolumic comparisons of Vmax serve as a reasonable indicator of changes in the relative degree of airway and parenchymal hysteresis.

Theophylline Minimally Inhibits Bronchoconstriction Induced by Dry Cold Air Inhalation in Asthmatic Subjects

The aim of this study was to evaluate the effect of a sustained-release theophylline preparation on bronchial responsiveness to cold dry air inhalation in asthmatic subjects. Sixteen adult subjects with asthma in a clinical steady state underwent 3 isocapnic cold air challenges on 3 consecutive days at a time when they had not received oral theophylline medication over the past 3 days. The dose of cold air causing a 20% (PD20) fall in FEV1 was obtained from each subject's dose-response curve. Subjects were then administered active or placebo sustained-release theophylline preparations according to a double-blind, randomized, two-treatment crossover design. Medication was given for a minimum of 3 consecutive days. PD20 was reassessed on 4 different days, 3 to 4 h after receiving active or placebo medication (two visits for each medication). We found a significant bronchodilator effect of theophylline as compared to the placebo (mean +/- SD differences in changes of FEV1 of 8.8 +/- 1.9%). We also documented a significant blocking effect of the active medication as opposed to the placebo on PD20 (p = 0.01). This difference (mean = 0.18 on the loge scale) was statistically beyond the intraindividual between-day variability observed on the 3 control days (p less than 0.001) but was physiologically minimal. This blocking effect was also partially related to changes in airway caliber. We conclude that theophylline showed a blocking effect on bronchial responsiveness to dry cold air, which was physiologically minimal and was partially related to changes in airway caliber.

Enhancing effect of dipyridamole inhalation on adenosine‐induced bronchospasm in asthmatic patients

The study was performed on 13 asthmatic patients to determine whether inhaled dipyridamole would act directly by inducing bronchoconstriction or indirectly by potentiating the adenosine-induced bronchoconstriction. The study was performed in 3 consecutive days. On the first day adenosine challenge was performed and the PD20 value calculated. On the other days the adenosine challenge was done 5 min after randomized inhalations of dipyridamole or a control solution. The mean percent change in FEV1 after dipyridamole (delta % = 2.0) and control solution (delta % = 1.0) was not significant. Inhaled adenosine caused bronchoconstriction with a geometric mean PD20 of 1.09 mg. After control solution inhalation, a mean PD20 value of 1.31 mg was observed. Dipyridamole inhalation increased adenosine hyperresponsiveness and in all subjects shifted the dose-response curves of adenosine challenge to the left with a mean PD20 value of 0.40 mg. This enhancing effect of dipyridamole was significant when compared with the baseline value (P less than 0.01) and control solution (P less than 0.01). The study demonstrated that dipyridamole inhalation increased airway responsiveness to adenosine in all subjects. This effect is due to indirect activity of dipyridamole on airways without changes in baseline airway caliber.

A longitudinal study of the occurrence of bronchial hyperresponsiveness in western red cedar workers.

Two hundred twenty-seven workers in a western red cedar sawmill underwent methacholine bronchoprovocation testing at least 2 times during 3 surveys over a 2-yr period. At the first survey, workers completed a respiratory and occupational questionnaire, performed spirometry, gave serum for measurement of plicatic acid-specific IgE antibodies by radioallergosorbent testing, and had skin prick tests to detect atopy. Bronchial hyperresponsiveness was present initially in 18% of the workers. Approximately 15% of those with initially no hyperresponsiveness developed hyperresponsiveness during the follow-up period; 15% of those with initial hyperresponsiveness also lost it during follow-up. Development of hyperresponsiveness tended to coincide with a decrease in level of pulmonary function, whereas loss of hyperresponsiveness was associated with improvement in pulmonary function. Workers with either persistent bronchial hyperresponsiveness or with varying responsiveness had a higher prevalence of plicatic acid IgE antibodies and lower levels of initial pulmonary function than did workers with persistent nonresponsiveness. Workers with persistent hyperresponsiveness had higher initial estimated total airborne dust exposure than did other workers. Age, duration of sawmill employment, atopy, race, and cigarette smoking did not influence the occurrence of hyperresponsiveness. Levels of plicatic-acid-specific IgE antibodies did not change substantially over the 2 yr. These results indicate that immunologic sensitivity to plicatic acid and change in airway caliber are associated with the occurrence of bronchial hyperresponsiveness in cedar workers.

Upper airway obstruction in infants and children: evaluation with ultrafast CT.

The diagnostic accuracy of ultrafast computed tomography (CT) was evaluated prospectively in 25 infants and children with suspected airway obstruction. All examinations were conducted in spontaneously breathing, nonsedated children. Scan acquisition times were 0.05 or 0.1 second. CT examinations, completed in an average of 10 minutes, routinely included localizing, contiguous sections through the trachea followed by serial images obtained at a rate of 17 per second through regions of interest. Imaging results were correct in 24 of 25 examinations as judged from clinical and surgical data. Ultrafast CT data permitted diagnosis of dynamic changes in airway caliber, small intraluminal polyps, focal tracheal atresia, compressive mediastinal masses, and foreign body obstructions of the major bronchi. Dose measurements showed a maximum skin exposure of 245 mR (0.06 mC/kg) per 0.05-second image. Ultrafast CT provides an accurate, minimally invasive method for dynamic imaging of the airway in nonsedated children.

The temporal relationship between increases in airway responsiveness to histamine and late asthmatic responses induced by occupational agents

The temporal relationship between increases in airway responsiveness and the late asthmatic response was assessed in nine patients challenged with occupational agents toluene diisocyanate (one patient), carmine (one patient), maleic anhydride (two patients), colophony (four patients), and trimellitic anhydride (one patient). The provocation concentration of histamine causing a 20% decrease in FEV 1 (PC 20) was measured before challenge and at approximately 3 hours and 24 hours on control and active-challenge days. Thirteen active challenges provoked eight definite late asthmatic responses (maximum fall in FEV 1 > 15% at 3 to 11 hours). At 3 hours after the challenges that provoked late responses, there was a significant ( p < 0.02) decrease in PC 20 that was more ( p < 0.03) than that observed for the five tests provoking early (late FEV 1 fall 0% to 5%) or equivocal late (FEV 1 fall 6% to 15%) responses. At 24 hours, PC 20 remained decreased ( p < 0.05), although it was less so than at 3 hours ( p < 0.05) and not significantly when compared with challenge tests causing single early or equivocal late responses. The 3-hour decreases in PC 20 were identified when FEV 1 (five of seven observations) was >90% of prechallenge values. For the nine independent tests, the 3-hour decreases in PC 20 correlated (r = 0.72; p < 0.05,) with the magnitude of the late falls in FEV 1, whereas this was not observed at 24 hours (r = 0.35; p, not significant). These results demonstrate that in subjects challenged with occupational agents, increases in histamine airway responsiveness precede the late asthmatic response, occur independently of changes in airway caliber, and correlate with the magnitude of the subsequent late response. We suggest that in subjects with occupational asthma, the late asthmatic response depends on the tissue events, possibly airway inflammation, that underlie the preceding increase in airway responsiveness.

Exposure to a sensitizing occupational agent can cause a long-lasting increase in bronchial responsiveness to histamine in the absence of significant changes in airway caliber

A 58-year-old subject with a history of occupational asthma to red-cedar sawdust underwent specific inhalation challenges with this product. Significant increases in airway responsiveness to histamine (tenfold fall in PC 20 FEV 1) were documented 7 hours after exposure for 5 minutes to red cedar while baseline spirometry remained unchanged. A dual asthmatic reaction was induced during the following days by exposing the subject to red-cedar sawdust for 30 minutes and plicatic acid for 7 minutes. After recovery of PC 20, the subject was reexposed to plicatic acid for 15 and 30 seconds on 2 consecutive days. No significant changes in FEV 1, forced vital capacity, and residual volume were demonstrated in the following 8 hours, although minimal changes in forced expiratory flow rate between 25% and 75% of FVC were observed. PC 20 dropped significantly and required 2 weeks to recover. This example illustrates that bronchial hyperresponsiveness to histamine can precede the changes in airway caliber after an antigen challenge. It also demonstrates that such changes can persist for up to 2 weeks after the challenge, even when no significant changes in FEV 1 are induced.

Late bronchial response and increase in methacholine hyperresponsiveness after exercise and distilled water challenge in atopic subjects with asthma with dual asthmatic response to allergen inhalation

We investigated the occurrence of late asthmatic response and increased methacholine responsiveness after exercise and ultrasonically nebulized distilled water (UNDW) inhalation in 12 subjects with asthma with dual asthmatic response and increased responsiveness after allergen challenge. On 3 separate days, allergen, exercise, and UNDW challenges were performed 2 hours after methacholine. FEV 1 was measured for 8 hours to detect any delayed change in airway caliber. If there were a further significant reduction in FEV 1 after the recovery from the immediate bronchoconstriction, methacholine challenge was performed again when FEV 1 had returned to baseline. Reproducibility of any observed late response to exercise and UNDW was also investigated by repeating these challenges on 2 subsequent days. After allergen inhalation only nine subjects had an early asthmatic response, whereas all the tested subjects demonstrated a late reaction and increased methacholine responsiveness. Ten subjects had an immediate response to exercise, and this was followed by a late response in only four patients. Nine subjects demonstrated early response to UNDW inhalation, and five subjects also had a late reaction. These late responses were associated with an increase in methacholine responsiveness in a subset of the tested subjects. Late-phase reactions to exercise and UNDW were not reproducible.

Increased neutrophil chemotactic activity in exercise- and "fog"-induced asthma.

To investigate whether exercise- and ultrasonic "fog"-induced asthma are due to the same mechanism, i.e. mediator release induced by osmotic changes, we measured the serum neutrophil chemotactic activity before and after exercise and inhalation of "fog" in 15 asthmatic subjects. To assess changes in airway caliber we measured specific airway conductance (SGaw); to assess changes in neutrophil chemotactic activity we measured the maximum distance reached by neutrophils in a filter when challenged with the subject's serum in a Boyden chamber. In 10 subjects, SGaw decreased by more than 35% and neutrophil chemotactic activity increased significantly (P less than 0.05) both after exercise and "fog", whereas in five subjects no change occurred either after exercise or "fog". We conclude that both exercise- and "fog"-induced asthma are associated with increased serum neutrophil chemotactic activity, and that both stimuli may cause asthma by osmotically triggering mediator release from mast cells.

Diurnal variation in bronchial responsiveness in asthmatic children

To establish the presence of a diurnal variation in bronchial responsiveness in asthmatic children, the increase of peak expiratory flow rate (PEFR) following sympathomimetic inhalation and the response to bronchial provocation with histamine and hyperventilation of cold dry air (HVCDA) were studied. Twenty-nine patients (20 boys, nine girls, aged 9.3 to 17.8 years) measured PEFR before and after sympathomimetic inhalation three times a day for four weeks. A further 15 patients (eight boys, seven girls, aged 6.9 to 18.0 years) underwent bronchial provocation testing every six hours for 24 hours. A diurnal variation in bronchodilator responsiveness was demonstrated in 55% of the first group. Mean amplitude was 60.8% of patients' mean increase in PEFR following bronchodilators. On grouped data, bronchodilation was greater in the morning than in the afternoon (p less than 0.0005) or in the evening (p less than 0.0005). A diurnal variation in the response to bronchial provocation was also found in the second group, but the timing of the rhythm depended on the stimulus used. On grouped data, airways were most sensitive to histamine at 0400 hours and most sensitive to HVCDA at 1600 hours. The diurnal variation demonstrated in bronchial responsiveness could not be attributed to changes in baseline airway caliber and was present, despite the patients' taking sufficient medication to control their asthmatic symptoms.

Medullary effects of nicotine and GABA on tracheal smooth muscle tone

Airway tone can be modulated centrally by the brain as well as by peripheral receptors. In part these changes in airway caliber seem to be secondary to changes in respiratory activity. Since structures near the ventrolateral medullary surface (VMS) can produce profound effects on respiration, it seems reasonable to believe that they might also be capable of modifying tracheal tone. In this study we examined the effects of two agents with respect to their action on tracheal tone; nicotine, a respiratory stimulant when applied to VMS, and gamma aminobutyric acid (GABA), a respiratory depressant when similarly administered. In chloralose anesthetized, paralyzed, artificially ventilated cats, tracheal tone was assessed by measuring pressure changes in a rostral bypassed of the trachea, while phrenic nerve activity was examined simultaneously. Nicotine administered on the intermediate area of the VMS both before and after carotid sinus denervation increased phrenic activity and induced constriction of the rostral tracheal segment. The response to nicotine could be blocked by application of a nicotine antagonist, hexamethonium, or prior local administration of lidocaine to the VMS. Activation of GABAergic receptors by application of GABA on the intermediate area of the VMS markedly reduced respiratory activity and nearly abolished the increased tracheal tone produced by inhalation of 7% CO 2 in O 2. The effects of GABA were eliminated by the prior administration to the VMS of bicuculline, a GABA receptor antagonist. These results indicate that structures located on the ventral surface of the medulla which affect breating may also play a significant role in the regulation of airway smooth muscle tone.

Theophylline partially inhibits bronchoconstriction caused by inhaled histamine in subjects with asthma

Sixteen adult subjects in a clinical steady state had four consecutive histamine inhalation tests on the same day when they were not receiving oral theophylline medication. The provocative concentration of histamine causing a 20% fall in FEV 1 (PC 20) was used to assess the response. They were then administered active or placebo sustained-release theophylline preparations according to a double-blind, randomized 4.4.1. two-treatment crossover design. Medication was administered for a minimum of 3 consecutive days, and PC 20 was reassessed on 4 different days, 3 to 4 hours after receiving active or placebo medication (two visits for each medication). A significant but small bronchodilator and blocking effect on histamine excitability was demonstrated for the active medication. This latter effect was present even by adjusting for changes in baseline airway caliber and for the intraindividual variability of the four PC 20 values obtained on day 1. We conclude that theophylline partially blocks bronchial responsiveness to inhaled histamine.

The Relationship between Seasonal Change in Non-Specific Bronchial Reactivity and Baseline Airway Calibre in a Community Population

Conference Abstract| January 01 1986 The Relationship between Seasonal Change in Non-Specific Bronchial Reactivity and Baseline Airway Calibre in a Community Population J.R. Britton; J.R. Britton 1City Hospital, Nottingham St Thomas' Hospital, London Southampton General Hospital Search for other works by this author on: This Site PubMed Google Scholar P.G.J. Burney; P.G.J. Burney 1City Hospital, Nottingham St Thomas' Hospital, London Southampton General Hospital Search for other works by this author on: This Site PubMed Google Scholar S. Chinn; S. Chinn 1City Hospital, Nottingham St Thomas' Hospital, London Southampton General Hospital Search for other works by this author on: This Site PubMed Google Scholar A.O. Papacosta; A.O. Papacosta 1City Hospital, Nottingham St Thomas' Hospital, London Southampton General Hospital Search for other works by this author on: This Site PubMed Google Scholar F. Anderson; F. Anderson 1City Hospital, Nottingham St Thomas' Hospital, London Southampton General Hospital Search for other works by this author on: This Site PubMed Google Scholar D. Pearson; D. Pearson 1City Hospital, Nottingham St Thomas' Hospital, London Southampton General Hospital Search for other works by this author on: This Site PubMed Google Scholar A.E. Tattersfield A.E. Tattersfield 1City Hospital, Nottingham St Thomas' Hospital, London Southampton General Hospital Search for other works by this author on: This Site PubMed Google Scholar Clin Sci (Lond) (1986) 70 (s13): 47P. https://doi.org/10.1042/cs070047Pa Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation J.R. Britton, P.G.J. Burney, S. Chinn, A.O. Papacosta, F. Anderson, D. Pearson, A.E. Tattersfield; The Relationship between Seasonal Change in Non-Specific Bronchial Reactivity and Baseline Airway Calibre in a Community Population. Clin Sci (Lond) 1 January 1986; 70 (s13): 47P. doi: https://doi.org/10.1042/cs070047Pa Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search nav search search input Search input auto suggest search filter All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. © 1986 The Biochemical Society and the Medical Research Society1986 Article PDF first page preview Close Modal You do not currently have access to this content.

Within-breath changes of airway calibre in patients with airflow obstruction by continuous measurement of respiratory impedance

We bench-tested a commercially available instrument for measuring respiratory impedance (Siregnost FD5: Siemens) and found that resistance ( R) and phase changes were accurately recorded in models. In a single human subject, total respiratory resistance ( R 1) was closely comparable to resistance measured by the Mead—Whittenberger technique. The derived continuous variable ( R os) was similar to R at <4 cmH 2O·litres −1·sec, but underestimated R at higher values. R os was highly correlated with airways resistance by body plethysmography ( R aw), but with a low slope and high intercept ( R os=1.38+0.59 R aw: r=0.89). Because of turbulence, both in model larynxes and in normal subjects, R os tends to rise with increases in flow in either direction. R os also tends to fall as lung volume rises, and vice versa, reflecting cyclic changes in airway calibre. We devised indices of expiratory narrowing of airways from the maximum flow-volume loop, and the plethysmographic alveolar pressure-flow loop, and compared them with the slope of the relation between R os and lung volume during tidal breathing, in nine normal subjects and 16 patients with airflow obstruction. Twelve of the 16 patients, all with abnormal flow-volume loops, had high R os-volume slopes, demonstrating excessive expiratory narrowing even during tidal breathing. We found no patients with normal inspiratory R os together with an abnormal R os - volume slope. Thus unstressed inspiratory calibre was never dissociated front airways narrowing on expiration.

Circadian variation in airway function

Nocturnal asthma is a common and troublesome problem. Many possible mechanisms have been proposed, including exposure to allergens, sleep itself, the supine posture, withdrawal of bronchodilator drugs, gastric reflux, mucus plugging, and airway cooling. Although these may be contributory factors in individual patients, they cannot provide a universal explanation for the phenomenon of nocturnal and early morning wheezing. It now seems that nocturnal asthma may best be understood in terms of circadian rhythms. A circadian variation in airway caliber has been demonstrated in normal subjects; in asthmatic subjects, the same rhythm is present but with greater amplitude. The amplitude is magnified by bronchial hyper-responsiveness, a cardinal feature of asthma. Evidence now suggests that the fall in circulating epinephrine level at night removes an important defense against bronchoconstriction in asthmatic subjects, and this itself may be magnified by removal of the braking effect of epinephrine on mast cell mediator release. In addition, increased vagal reflex bronchoconstriction and the delayed effects of the fall in plasma cortisol level may also contribute to nocturnal wheezing. Thus, nocturnal asthma may be explained by a complex interaction of several coincident circadian rhythms, which produce only small changes in airway caliber in normal subjects; however, in asthmatic patients, these constrictor effects are magnified to produce bronchospasm severe enough to wake the patient.

TRACHEAL DIAMETERS AND DYNAMICS IN INFANTS AND CHILDREN MEASURED BY CINE-CT

Nine children were evaluated for tracheal obstruction by having their intra- and extra-thoracic tracheal diameters measured using Cine-CT. The patients ranged in age from one month to four years, and had clinical signs and symptoms of respiratory distress with stridor. They entered a protocol in which there was full clinical evaluation, and in some, measurement of esophageal pressures and tidal breathing flowvolume loops. The patients were scanned without sedation using a Cine-CT scanner (Imatron, Inc., CA) which provided eight level image acquisition in 240 msec without moving the patients. Using the scanner in the “Cine” mode, 13 to 20 slices obtained over 1 to 2 respiratory cycles were obtained at several levels of both the intra-and extra-thoracic trachea to detail dynamic changes in airway caliber. Images were obtained at relatively low dose and were reconstructed in 14 seconds. Cross-sectional areas of the trachea were obtained by planimetry, and saggital and coronal tracheal diameters directly measured. The clinical and laboratory data correlated well with the imaging measurements, and were compared with Age-related normal Cine-Ct tracheal diameters, and published post-mortem airway caliber data. We conclude that Cine-CT is a rapid method for tomographic evaluation of tracheal dynamics that can be employed for children without sedation.

Effect of beclomethasone dipropionate on bronchial responsiveness to histamine in controlled nonsteroid-dependent asthma

We investigated the possibility that corticosteroids can reduce bronchial responsiveness to histamine by mechanisms other than change in airway caliber. Ten adult asthmatic subjects were selected because their symptoms were controlled by bronchodilators alone, they had no recent respiratory infection or allergen exposure that might have temporarily altered responsiveness, their spirometry was more than 70% predicted, and they had a range of histamine bronchial hyperresponsiveness. They received, in random order and double-blind manner, beclomethasone dipropionate (400 μg daily) or placebo for 4 wk and then, after a 2-week washout period, they crossed over to the other treatment for 4 wk. Treatment, with beclomethasone induced a small but significant reduction in bronchial responsiveness to histamine ( p = 0.014). Although the improvement was too small to be considered of clinical significance, its importance lies in the mechanisms by which it was produced. Part of the improvement was related to improvement in airway caliber, but, even when the data was adjusted for this, there was still a significant difference between beclomethasone and placebo treatment (p = 0.018). The results suggest that regular treatment with corticosteroids can alter bronchial responsiveness through mechanisms other than change in airway caliber.