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PubMed1992

Oxatomide modifies methacholine- and exercise-induced bronchoconstriction in asthmatic children.

Oxatomide is a potent inhibitor of both the release and effects of allergic mediators and is similar to calcium antagonists in chemical structure. It prevents histamine release by inhibiting not only the increase in calcium intake, but also intracellular calcium release. We investigated its effect on methacholine-induced and exercise-induced bronchoconstriction in asthmatic children. Methacholine challenges were performed after oral administration of 0.88 mg/kg oxatomide or placebo in nine asthmatic children in a double-blind placebo-controlled study. Respiratory thresholds were improved in seven patients and log PC20 in the oxatomide group (6.65 +/- 1.34 micrograms/mL) was significantly higher than that in the placebo group (5.74 +/- 1.04 micrograms/mL) (P < .05). Exercise challenges were performed after oral administration of 1.5 mg/kg oxatomide or placebo in eight asthmatic children in a double-blind placebo-controlled study. Oxatomide produced acute bronchodilatation with 6.1% improvement on an average in FEV1. The mean maximal % fall obtained by oxatomide was 13.5%, while that by placebo was 22% (P < .05). These results indicate that oxatomide reduces nonspecific bronchial hyperresponsiveness.

Adolescent↗
PubMed1992

The effects of indomethacin on the refractory period to hypertonic saline-induced bronchoconstriction.

The purpose of this study was to determine the effect of pretreatment with indomethacin on the refractory period to hypertonic saline-induced bronchoconstriction. In a double-blind, placebo-controlled, randomized trial nine asthmatic subjects underwent two hypertonic saline challenges, 60 min apart, on a control day and after premedication with indomethacin 50 mg or matching placebo, twice daily for three days. Premedication with indomethacin did not change airway responsiveness to the initial hypertonic saline challenge. The mean maximal % fall in specific airway conductance (sGaw) was 40.3, 44.1 and 47.6% on the control, placebo and indomethacin days, respectively. Subjects were significantly less responsive to the second hypertonic challenge as compared to the initial challenge on all three study days. There was a variable effect of indomethacin pretreatment on the refractory period. Five subjects lost their refractory period after indomethacin, when the variability of the test was taken into account. This suggests that there may be contributory mechanisms to the refractory period other than the release of protective prostanoid metabolites.

Adolescent↗
PubMed2005

[The effect of montelukast, a leukotriene antagonist, on improvement of exercise-induced bronchoconstriction].

OBJECTIVE: To study the efficacy of montelukast, a cysteinyl leukotriene receptor antagonist, in the treatment and prevention of exercise-induced bronchoconstriction (EIB) in mild asthmatic patients and patients with exercise-induced asthma (EIA). METHODS: Thirty mild asthmatic patients with positive standardized exercise challenge test were enrolled. The subjects received montelukast 10 mg once daily in the evening. Standard exercise challenge was performed before, three days and twenty-eight days after the administration of the drug. The end points included: (1) Area under the percent fall in forced expiratory volume in one second (FEV1) versus time curve (AUC0 to approximately 60 min); (2) Time of recovery to within 5% of the pre-exercise baseline FEV1 value; and (3) Maximal percent fall in FEV1 from pre-exercise baseline. RESULTS: Montelukast caused significant reduction in AUC0 to approximately 60 min, which was (39 +/- 21)%.min before treatment as compared to (13 +/- 14)%.min and (12 +/- 14)%.min three days and twenty-eight days respectively after the treatment with montelukast. Time of recovery to within 5% of the pre-exercise baseline FEV1 value were (51 +/- 36) min, (26 +/- 28) min and (25 +/- 33) min respectively. The mean maximal percentage decrease in FEV1 after exercise was 44.4% before treatment, 26.8% and 18.2% following montelukast. FEV1 and peak expiratory flow rate (PEFR) were maintained to nearly normal during all the study. Inhale corticosteroid did not prevent EIB/EIA. CONCLUSION: Montelukast attenuates and protects against EIB/EIA.

Acetates↗
PubMed1992

Repeated inhalation of bradykinin attenuates adenosine 5'-monophosphate (AMP) induced bronchoconstriction in asthmatic airways.

Repeated bronchial challenges with inhaled bradykinin lead to a rapid loss of the bronchoconstrictor response and this has been suggested to be due to depletion of contractile neuropeptides from sensory nerve endings. If adenosine 5'-monophosphate (AMP), another potent bronchoprovocant in asthma, and bradykinin share a common pathway in inducing bronchoconstriction in asthmatic subjects, then repeated bradykinin bronchoprovocation tests should reduce the response to subsequent inhalation of AMP. We examined this hypothesis in eight asthmatic subjects in a double-blind, randomized study. On the histamine study day, two consecutive concentration-response studies with inhaled histamine were followed by a third consecutive challenge with AMP and the provocation concentration producing a 20% fall in forced expiratory volume in one second from the post-diluent baseline value (PC20 FEV1) for this agonist was calculated. On the bradykinin study day, two consecutive bronchoprovocation tests with bradykinin were followed by a third inhalation challenge to obtain the PC20AMP value. On a further occasion, the asthmatic subjects underwent two consecutive concentration-response studies with inhaled bradykinin followed by a third consecutive challenge with histamine. On the histamine study day, the geometric mean PC20AMP value was 28.1 mg.ml-1, whilst on the bradykinin study day, the fifteenfold reduction in bradykinin responsiveness after the second bradykinin challenge was accompanied by a significant reduction of the airway responsiveness to AMP, the PC20AMP being 59.8 mg.ml-1. A similar reduction in bradykinin responsiveness failed to alter the airway response to a subsequent inhalation with histamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Monophosphate↗
PubMed1991

Possible roles of the peripheral vagal nerve in histamine-induced bronchoconstriction in guinea-pigs.

Although the importance of the vagal nerve in the pathogenesis of bronchial asthma has been reported, its precise contribution is still not fully understood. To shed more light on this area, we evaluated the possible contribution of vagal reflex in histamine-induced bronchoconstriction (HIB), and decided the site of action of histamine on the vagal nerve. For this purpose, we studied the effects of the bilateral cervical vagotomy, hexamethonium (2 mg.kg-1) or tetrodotoxin (0.5 mg.kg-1) on HIB (8 micrograms.kg-1, iv) in anaesthetized and mechanically-ventilated guinea-pigs. We also studied whether or not atropine (1 mg.kg-1) decreases HIB after vagotomy, including either the treatment of hexamethonium or tetrodotoxin. Airway responses were assessed by measurement of pulmonary resistance. The following results were obtained; 1) the response to histamine was significantly enhanced by the vagotomy, hexamethonium or tetrodotoxin; 2) propranolol increased HIB, and HIB was further enhanced by the vagotomy in the animals treated with propranolol; 3) atropine significantly suppressed HIB after the vagotomy, hexamethonium or tetrodotoxin. These results suggest that the postganglionic vagal nerve plays an excitatory role in HIB through the release of acetylcholine from the nerve terminals. It is also suggested that the vagal reflex mainly exhibits an inhibitory role in the HIB of guinea-pigs, presumably by the action of the nonadrenergic inhibitory nervous system.

Animals↗
PubMed1991

Effect of the new antiallergic drug epinastine on chemical mediator induced bronchoconstrictions in guinea pigs.

Recently, mast cell stabilizers, so called antiallergic drugs, that also have blocking effects on receptors for chemical mediators (CM) have been developed. The present study investigated the effects of a new antiallergic drug, epinastine (3-amino-9,13b-dihydro-1H-dibenz[c,f]imidazol [1,5-a]azepine hydrochloride, WAL 810 CL; CAS 80012-43-7) on the in vivo bronchoconstriction (BC) induced by several CM as compared with those of other antiallergic drugs such as ketotifen, azelastine and oxatomide. Male Hartley guinea pigs were used. The BC was measured with a modified Konzett-Rössler method and expressed as a change in ventilation overflow (VO) under anesthesia. Antiallergic drugs were given orally 1 h before i.v. administration of CM. I.v. administrations of histamine (His), U-46619 (thromboxane A2 mimetic), leukotriene D4 (LTD4), prostaglandin D2 (PGD2), substance P (SP), neurokinin A (NKA), bradykinin (BK) and endothelin-1 (ET-1) increased VO in a dose dependent manner. The potency was as follows; ET-1 greater than LTD4 greater than NKA much greater than U-46619 greater than SP greater than His greater than BK much greater than PGD2. All the antiallergic drugs used markedly inhibited the His-induced BC. Epinastine, ketotifen and azelastine also significantly inhibited the BK-induced BC; epinastine had the strongest anti-BK effect among them. On the other hand, the four antiallergic drugs did not inhibit the BC induced by the other CM except for His and BK. Based on the above results, it is suggested that epinastine possesses anti-His and BK effects, and therefore could be promising as a new antiallergic drug without sedative effect.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1992

Thromboxane A2 accounts for bronchoconstriction but not for platelet sequestration and microvascular albumin exchanges induced by fMLP in the guinea pig lung.

When injected i.v. to guinea pigs, the granulocyte secretagog N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP) induces bronchoconstriction (BC), lung platelet sequestration and increased transendothelial albumin exchanges in lungs. We evaluated BC and the variations of the lung contents in radiolabeled platelets, erythrocytes and extravascular albumin, as measurements of platelet lung entrapment, reduction of lung blood volume and increase of transendothelial albumin exchanges, respectively. Trimetoquinol, a thromboxane A2 (TXA2)-endoperoxide receptor antagonist, inhibited BC and platelet entrapment by lungs induced by fMLP, but protection was nonspecific because it also suppressed BC by histamine. The specific TXA2 synthetase inhibitor/endoperoxide receptor antagonist ridogrel suppressed BC and reduced lung platelet entrapment, but failed to prevent the increase of extravascular albumin and the decrease of erythrocyte lung contents due to fMLP. Consequently, the fMLP-induced increase of vascular albumin exchanges and reduction of lung blood volume are TXA2-independent. Aspirin prevented BC, but failed to suppress lung platelet entrapment by fMLP, indicating that in vivo platelet activation is not TXA2-dependent, even though the levels of circulating TXB2, the stable metabolite of TXA2, were increased after fMLP concomitantly with that of 6-keto-prostaglandin (PG)F1 alpha, the stable metabolite of PGI2. The ridogrel-treated animals showed reduced blood level of TXB2 and increased levels of 6-keto-PGF1 alpha after fMLP challenge. Blocking the cyclooxygenase pathway with aspirin prevented ridogrel-induced protection against lung platelet sequestration after fMLP, supporting the concept that rechanneling of arachidonate metabolism toward protective prostaglandins accounts for protection by ridogrel.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1992

Combined effect of nifedipine and diltiazem on methacholine-induced bronchoconstriction in asthmatic patients.

Calcium blockers alter airway hyperreactivity. We studied the effect of either 60 mg diltiazem or 20 mg nifedipine and their combination on the airway response to methacholine-induced bronchoconstriction. Compared with placebo or diltiazem, nifedipine significantly raised the PC20. When diltiazem was given alone, it had no effect on the airway but, when given with nifedipine, it significantly raised the PC20 to methacholine. The effect was superior to any of the other treatments given. This study supports the concept of combining two different calcium blockers in the treatment of bronchial asthma.

Adolescent↗
PubMed1991

The effects of a 5-lipoxygenase inhibitor on antigen-induced mediator release, late-phase bronchoconstriction and cellular infiltrates in primates.

Inhaled BI-L-239 significantly inhibited i-LTC4 generation, late-phase bronchoconstriction and the influx of neutrophils into the lungs. We conclude that leukotriene generation and release within the lungs, following allergen exposure, in part mediate altered lung function and contribute to the development of airway inflammation. As such, treatment with a selective 5-lipoxygenase inhibitor may aid in the treatment of bronchial asthma and other allergic diseases.

Administration, Intranasal↗
PubMed1991

A pharmacologic examination of receptors mediating serotonin-induced bronchoconstriction in the anesthetized guinea pig.

The receptors involved in the bronchoconstriction evoked in vivo by intravenous administration to the anesthetized guinea pig of serotonin and serotonin-related agonists have been examined in this study. Animals were pretreated with indomethacin and (+/-)-propranolol to inhibit cyclooxygenase and beta adrenergic receptors, respectively, and pulmonary parameters were obtained with a Buxco pulmonary mechanics computer. Dose-dependent increases in pulmonary resistance and decreases in dynamic lung compliance were produced by serotonin, 2-methyl-serotonin, 5-methoxy-tryptamine, alpha-methyl-serotonin, 5-carboxamidotryptamine, and m-trifluoromethylphenylpiperazine (TFMPP). Responses to all agonists except 2-methyl-serotonin, a selective 5-hydroxytryptamine3 (5-HT3) agonist, were antagonized by the 5-HT2 antagonists, LY53857 and ketanserin. Zaclopride, 1 and 10 mg/kg, a selective 5-HT3 antagonist, blocked responses to 2-methyl-serotonin. A maximally effective dose of LY53857 (1 mg/kg) produced larger shifts of the dose-response curves to serotonin, 5-methoxytryptamine and alpha-methyl-serotonin than did a maximally effective dose of ketanserin (1 mg/kg). Thiorphan, 10 mg/kg, an inhibitor of neutral endopeptidase, potentiated 2-methyl-serotonin and, when studied in the presence of LY53857, also potentiated serotonin, 5-methoxytryptamine and TFMPP. After thiorphan and LY53857, responses to serotonin, but not 5-methoxytryptamine or TFMPP, were blocked by zaclopride. Capsaicin pretreatment of the animals resulted in rightward shifts of the dose-response curves to serotonin, 2-methyl-serotonin and TFMPP, but not to 5-methoxytryptamine or alpha-methyl-serotonin. Potentiation by thiorphan and antagonism by zaclopride of responses to serotonin were still evident after capsaicin pretreatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1991

Bombesin-induced bronchoconstriction in the guinea pig: mode of action.

Bombesin is a potent bronchoconstrictor in guinea pigs in vivo, but the mechanisms of its effect are not certain. In vivo increases in tracheal pressure induced by bombesin were measured as an index of airway caliber. Bombesin (0.3-10 micrograms/kg) produced a dose-related bronchoconstrictor response in vivo which was not inhibited by indomethacin (5 mg/kg), BW A4C (50 mg/kg, a lipoxygenase inhibitor), WEB 2086 (10 micrograms/kg, a platelet-activating factor antagonist) or mepyramine (10 mg/kg, a histamine H1-receptor antagonist). Capsaicin pretreatment (50 mg/kg), which depletes neuropeptides from sensory nerve endings, similarly failed to inhibit the action of bombesin. Propranolol (1 mg/kg) produced a small shift to the left and atropine (1 mg/kg) and the serotonin antagonist, methysergide (1 mg/kg), produced a small shift to the right in the bombesin dose-response curve. The bombesin receptor antagonist, BIM 26159 (50 micrograms/kg), transiently inhibited bombesin-induced bronchoconstriction. Isoproterenol (0.1-10 micrograms/kg) reversed the increase in tracheal pressure induced by bombesin, suggesting that contraction of airway smooth muscle was involved. Bombesin (10(-10)-3 x 10(-5) M) failed to produce contraction in trachea or main bronchi either denuded of epithelium or in tissues pretreated with phosphoramidon, captopril or indomethacin (all 10(-5) M) and was inactive in peripheral lung strip preparations. Thus, bombesin is a potent constrictor of guinea pig airways in vivo. The inability of bombesin to contract airway smooth muscle in vitro suggests that the bronchoconstrictor action of bombesin is largely due to the release of an unidentified spasmogenic substance.

Animals↗
PubMed1990

Measuring the bronchial effects of bronchodilating drugs in healthy subjects with methacholine provocations: theophylline protects against induced bronchoconstriction in a dose-dependent manner.

To assess whether it would be possible to use methacholine (MCH) provocation tests with healthy subjects in the evaluation of bronchodilatory drugs, an intravenous infusion of theophylline ethylenediamine in increasing doses of 2.5, 5.0 and 7.5 mg/kg was given in random order to nine healthy non-smoking volunteers in a single-blind, placebo-controlled study. Dose response slope (DRS = maximal decline [%] in pulmonary function/the maximum dose of MCH [mumol]) was used to estimate airway reactivity. DRS was calculated to FEV1 (DRSFEV1) and to area under the flow-volume curve (AEFV, DRSAEFV). The bronchial reactivity was first tested with a standard MCH provocation method. An abbreviated, single-dose, method was used in the measurement of the effects of theophylline. The DRS-values obtained from the short method did not differ from those obtained from the standard one (p = 0.86, for DRSFEV1 and DRSAEFV), and correlation between these two methods was good (r = 0.93 and 0.98 for DRSFEV1 and DRSAEFV, respectively [p less than 0.001]). Serum theophylline concentrations achieved were (mean +/- SEM) 32.4 +/- 0.9, 63.7 +/- 3.3 and 93.4 +/- 3.3 mumol/l, which differed significantly from each other (p much less than 0.001). An inverse linear relationship between the serum theophylline concentration and the airway reactivity was observed with both indexes (r = -0.54, p less than 0.01 for DRSFEV1 and r = -0.65, p less than 0.001 for DRSAEFV). Even the lowest dose, which produced serum concentrations well under the therapeutic range, protected significantly (p less than 0.05) against MCH induced bronchoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Bronchial challenge to house dust can induce immediate bronchoconstriction in allergic asthmatic patients.

The goal of the study was to evaluate whether natural exposure to house dust could elicit immediate bronchoconstriction. Two groups of asthmatic patients were studied: 12 asthmatics allergic to house dust mites and seven nonallergic asthmatics. The baseline FEV1 was similar in the two groups. Each subject was challenged through a nasal mask connected to nebulizer filled with house dust. Patients were randomly assigned to inhale dust with high or low Group I allergenic level. All allergic patients had an FEV1 drop larger than 20% of the baseline value. This drop was maximal at the 30th minute after challenge. FEV1 remained unchanged in nonallergic asthmatics. Allergic patients challenged with high Group I allergenic house dust (8.4 micrograms/g) had a mean FEV1 drop larger (P less than .01) than those challenged with the low Group I allergenic house dust (0.66 micrograms/g). Late asthmatic reactions were found in only two patients who were challenged with the high Group I allergenic house dust. These two patients had immediate FEV1 drops greater than 50% of the baseline value. Occurrence of symptoms during the test and the drop in FEV1 were correlated (r = .3; P less than .05). Natural exposure to house dust can induce immediate bronchial in allergic asthmatics in a dose-dependent manner.

Adult↗
PubMed1994

Modulation of nonadrenergic noncholinergic neural bronchoconstriction by bradykinin in anesthetized guinea pigs in vivo.

The modulatory effect of bradykinin on excitatory nonadrenergic noncholinergic (e-NANC) neural constrictor responses was examined in anesthetized guinea pig airways in vivo. e-NANC responses were obtained by bilateral vagal stimulation in the presence of atropine (1 mg/kg i.v.) and propranolol (1 mg/kg i.v.). Indomethacin (5 mg/kg i.v.) and captopril (1 mg/kg i.v.) were pretreated to avoid the indirect effects of bradykinin by producing prostaglandins and to prevent endogenous breakdown of bradykinin, respectively. Bradykinin (0.01-1 nmol/kg i.v.) potentiated e-NANC responses in a dose-dependent manner. The potentiation was significant with 0.1 and 1 nmol/kg of bradykinin, 22.7 +/- 3.2% (mean +/- S.E.; P < .01) and 34.5 +/- 4.7% (P < .01), respectively), compared with that in sham-injected control animals (-4.7 +/- 3.6%). The potentiation of e-NANC responses by bradykinin (1 nmol/kg i.v.) was abolished by the subsequent administration of a bradykinin B2 receptor antagonist, HOE140 (0.1 mumol/kg i.v.), that was without effect on e-NANC responses by itself. The contraction induced by exogenous administration of substance P (1 nmol/kg i.v.) was not affected by the same dose of i.v. bradykinin; the change in substance P-induced bronchoconstriction was 9.2 +/- 8.3% with and 3.2 +/- 3.6% without bradykinin (P > .05). These results suggest that bradykinin potentiates e-NANC responses in guinea pig airways in vivo via B2 receptors which are possibly on prejunctional sites.

Animals↗
PubMed1994

Influence of theophylline on both bronchoconstriction and plasma extravasation induced by acetaldehyde in guinea-pigs.

Acetaldehyde administered intravenously at various doses (20, 40 and 80 mg/kg) elicits a dose-dependent increase in intratracheal pressure (ITP) and a proportional rise in histamine blood concentration in anaesthetized guinea-pigs. Similar effects were observed in ovalbumin-sensitized guinea-pigs upon aerosol of acetaldehyde (20 mg/ml) which has been administered at the flow rate of 0.1 ml/min for 2 min. Theophylline (CAS 58-55-9) antagonized both the increase of ITP values and the rise of histamine in the blood caused by acetaldehyde given intravenously (ED50 = 5.8 mg/kg i.v.) or by aerosol (ED50 = 4.9 mg/kg i.v.). Furthermore, in animals where combined treatment with pyrilamine (2 mg/kg i.v.) and captopril (2 mg/kg i.v.) resulted in a remarkable potentiation of the bronchoconstrictor response to acetaldehyde (20 mg/kg i.v.), the administration of theophylline (5 mg/kg i.v.) or of the substance P (SP) receptor antagonist, [D-Pro4, D-Trp7.9] SP 4-11 (10 mg/kg i.v.) reduced the augmented action of acetaldehyde on respiratory airways induced by captopril by more than 50%. Moreover, the bronchoconstriction induced by acetaldehyde (40 mg/kg i.v.) was also associated with a significant increase of extravasation of Evans blue in tracheal tissue. Both these effects of acetaldehyde were inhibited by theophylline (10 mg/kg i.v.), whereas a NK1-TK (neurokinin 1-tachykinin) receptor antagonist (412 micrograms/kg i.v.) reduced (81%; p < 0.001) only the vascular permeability changes caused by acetaldehyde.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaldehyde↗
PubMed1995

[Effect of loratadine, selective antagonist of histamine H1 receptors, on histamine-induced bronchoconstriction].

The aim of this study was to assess the duration of Loratadine effect on histamine H1 receptor in the airway. Six patients with mild or moderate asthma were examined. Bronchial reactivity to histamine was measured according to Cockcroft. The significant blockade of histamine H1 receptors in airway was observed from the 2nd day when 10 mg of Lo was given daily. The maximal protection with 10 mg doses was observed after 3-4 days. After another 5-6 days without Loratadine bronchial responsiveness return to the initial values. Single dose of 30 mg Loratadine given better protection against histamine bronchoconstriction than 10 mg given for 5 days. This effect was observed as early as 60 minutes after administration of Loratadine.

Adult↗
PubMed1994

[A case of aspirin-induced cough without bronchoconstriction. A new type of aspirin hypersensitivity].

A 54-year-old woman was admitted to our hospital because of an asthmatic attack. Her first asthma attack occurred when she was 53 years old. It was followed by a flu-like infection, and was preceded for one year perennial rhinitis and loss of the sense of smell. Symptoms were perennial, and unrelated to the seasons. Because these clinical findings resembled those of aspirin-induced asthma (AIA), an aspirin-DL-lysine i.v. challenge test was done. Cough, perspiration, and flushing was provoked within 15 min after aspirin-DL-lysine injection, but FEV1 did not change. Respiratory sounds were normal and no wheezing was audible. Other cyclooxygenase inhibitors (ketoprofen, sulpyrine and acetaminophen) provoked the same symptoms. Successively increasing doses of injected aspirin-DL-lysine resulted in complete tolerance to this stimulus. We propose that aspirin-induced cough without bronchoconstriction is a new type of aspirin hypersensitivity.

Aspirin↗
PubMed1994

Lung volumes and expiratory flow during bronchoconstriction in asthma.

Bronchial asthma is characterized by excessive airway narrowing and hyperinflation. In this review, the mechanisms linking the increases of functional residual capacity (FRC) and residual volume (RV) to reduced airway calibre are analysed. The authors have shown that the increase in FRC is closely associated with the occurrence of flow limitation, i.e. the achievement of maximum flow during tidal volume; whereas, the increase in RV can be modulated by the magnitude of the bronchodilator effect of the deep inhalation during induced bronchoconstriction. It can be speculated that flow limitation contributes to the increase in FRC through a reflex mechanism; whereas, the increase in RV depends on the site of airway narrowing, which in turn determines the relationship between airway and parenchymal properties.

Asthma↗