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PubMed1978

Bronchoconstrictive suggestion in asthma: a role for airways hyperreactivity and emotions.

Using whole-body plethysmographic measurements, asthmatic patients inhaled aerosolized saline presented either as a neutral substance (day 1) or in the guise of a bronchoconstrictor (day 2). Bronchoconstrictive suggestion resulted in increased airway resistance and decreased specific airway conductance, whereas thoracic gas volume was unchanged. The variation in the response was analyzed in relation to airways hyperreactivity, as indexed by methacholine and histamine inhalation challenges, and physiologic measures of the emotional reaction to bronchoconstrictive suggestion, as indexed by changes in blood pressure, heart rate, finger pulse amplitude, and forehead electromyographic activity. It was found that the bronchoconstrictive response was significantly related to the degree of airways hyperreactivity and to the emotional response. These results suggest that asthmatic patients apt to respond to bronchoconstrictive suggestion with airways obstructions are characterized by highly hyperreactive airways. Responders also appear to be emotionally labile, although it is not yet clear whether the emotional response per se evokes airway obstruction or is merely a by-product of the occurrence of airway obstruction.

Adolescent↗

PubMed1978

The beneficial effect of nasal breathing on exercise-induced bronchoconstriction.

In the first step of a study of the relation of nasal and oral breathing during moderate treadmill exercise to the onset of bronchoconstriction in young patients with perennial bronchial asthma, it was observed that most subjects spontaneously breathed with their mouths open when instructed to breathe "naturally." Subsequently, when they were required to breathe only through the nose during the exercise, an almost complete inhibition of the postexercise bronchoconstrictive airway response was demonstrated. When instructed to breathe only through the mouth during exercise, an increased bronchoconstrictive airway response occurred, as measured by spirometry, flow-volume relationships, and body plethysmography. These findings suggest that the nasopharynx and the oropharynx play important roles in the phenomenon of exercise-induced bronchoconstriction.

Adolescent↗

PubMed1981

Exercise increases sulfur dioxide-induced bronchoconstriction in asthmatic subjects.

We undertook a study to determine whether moderate exercise modifies the bronchoconstriction produced by sulfur dioxide (SO2) in subjects with mild asthma. In 7 subjects, we compared the changes in specific airway resistance (SRaw) produced by 10 min of exercise alone (400 kpm/min on a cycle ergometer), inhalation of SO2 alone, and the combination of exercise and SO2. During all studies, a subject breathed SO2 and/or air from a mouthpiece. In 6 additional subjects, we compared the increase in SRaw produced by inhalation of SO2 during exercise with that produced by eucapnic hyperventilation with SO2. Neither inhalation of 0.05 ppm of SO2 at rest nor exercise or hyperventilation alone had any effect on SRaw. Inhalation of SO2 during exercise, however, significantly increased SRaw (from 8.46 +/- 3.58 L x cm H2O/L/s (mean +/- SD) to 18.16 +/- 10.05 at 0.05 ppm and from 8.07 +/- 2.69 to 10.48 +/- 4.49 at 0.25 ppm (p less than 0.05)). In the 2 most responsive subjects, inhalation of 0.10 ppm of SO2 during exercise also significantly increased SRaw. The SRaw increased by the same amount whether SO2 was inhaled during exercise or during eucapnic hyperventilation at the same minute ventilation, but the time course of the increase in SRaw was different. The SRaw was at or near maximal values at the first measurement (30 s) after hyperventilation but not until 2 to 4 min after exercise. When 4 subjects took larger breaths after inhaling SO2 during eucapnic hyperventilation to more closely match the volume of the breaths taken after exercise, the time courses of SO2-induced bronchoconstriction after hyperventilation and after exercise were nearly identical. These results suggested that exercise increases the bronchoconstriction produced by a given concentration of SO2 in subjects with asthma by increasing the minute volume of ventilation and that the delay in bronchoconstriction after exercise is due to the large tidal volumes that persist for some minutes during recovery.

Adult↗

PubMed1981

Inhibition of sulfur dioxide-induced bronchoconstriction by disodium cromoglycate in asthmatic subjects.

To determine whether disodium cromoglycate (cromolyn) inhibits the bronchoconstriction produced by inhalation of sulfur dioxide (SO2) in people with asthma, we undertook a study of 6 asthmatic subjects. Each subject inhaled 40 mg of cromolyn on one day and lactose placebo on another day 20 min before inhaling SO2 for 10 min while exercising at a moderate rate (400 kpm/min) on a bicycle ergometer. Sulfur dioxide was delivered in humidified air at ambient temperature in concentrations of 0.5 ppm (3 subjects) or 1.0 ppm (3 subjects). Cromolyn and lactose treatments were given to each subject in a randomized sequence and in a double-blind manner. On a third day, each subject exercised at the same work rate breathing humidified air without SO2 at ambient temperature. We measured specific airway resistance (SRaw) in a body plethysmograph every 30 s for 10 min before and after each of the 3 periods of exercise. After treatment with lactose, SO2 inhalation significantly increased SRaw in all 6 subjects (from a baseline of 6.5 +/- 0.9 to 19.0 +/- 4.8 L x cm H2O/L/s (mean +/- SE) after SO2). After treatment with cromolyn, SO2 inhalation caused no increase in SRaw in 4 subjects and a small rise in 2 subjects. The mean increase in SRaw (from a baseline of 7.3 +/- 0.9 to 10.0 +/- 1.5 L x cm H2O/L/s after SO2) was significantly smaller than after lactose treatment (p less than 0.025). Exercise alone had no effect on SRaw in any subject. Thus, cromolyn inhibits SO2-induced bronchoconstriction in subjects with asthma. This finding suggests either that SO2 induces bronchoconstriction by stimulating the release of mediators from mast cells or that cromolyn inhibits bronchoconstriction by a mechanism independent of its effect on mast cells.

Adult↗

PubMed1983

Modification of allergic bronchoconstriction by a calcium antagonist: mode of action.

Because both degranulation of mast cells and contraction of airway smooth muscle are dependent upon the influx of calcium, a calcium blocking agent might modify allergic bronchoconstriction by at least these two mechanisms. We treated sheep allergic to Ascaris suum antigen with the calcium antagonist Verapamil prior to airway challenge with an aerosol of Ascaris suum antigen and also investigated the response without pretreatment. Aerosolized Ascaris suum antigen increased mean pulmonary resistance (RL) to 530% of baseline (n = 6). Pretreatment with intravenously administered Verapamil (150 micrograms/kg) increased mean RL to 225% of baseline but bronchoconstriction produced by subsequent antigen challenge was completely prevented. Verapamil did not modify bronchoconstriction produced by aerosols of histamine and carbachol, agents that act upon airway smooth muscle. Further, it did not reverse the increase in RL induced by an intravenous infusion of carbachol. These results suggest that verapamil, at the dosage used, did not prevent allergic bronchoconstriction by a direct action on smooth muscle and therefore was effective by inhibiting the release of mast cell mediators.

Airway Resistance↗

PubMed1984

Adenosine-induced bronchoconstriction in asthma. Antagonism by inhaled theophylline.

Inhaled adenosine causes bronchoconstriction in asthmatic patients. Antagonism of the bronchoconstrictor effect of endogenous adenosine has been proposed as a possible mechanism of action of theophylline in asthma. To directly investigate this, we have compared the airway responses to inhaled adenosine and histamine, with and without the prior administration of inhaled theophylline in 8 allergic asthmatic subjects. Airway response was measured both as forced expiratory volume in one second (FEV1) and as specific airway conductance (SGaw). Inhaled adenosine was less potent than histamine in producing bronchoconstriction, with geometric mean concentrations required to produce a 20% fall of FEV1 (PCf20) and a 40% fall of SGaw (PCs40) being 0.27 and 0.25 mg/ml for adenosine and 0.10 and 0.09 mg/ml for histamine. In a total nebulized dose of 37.5 mg, inhaled theophylline was a weak bronchodilator that caused maximal increases in FEV1 of 2 +/- 2% (mean +/- SE, p less than 0.05) and in SGaw of 8 +/- 4% (p greater than 0.05). However, theophylline significantly inhibited adenosine-induced bronchoconstriction, increasing the PCf20 and PCs40 values for adenosine to 1.66 (p less than 0.001) and 2.34 (p less than 0.005) mg/ml, respectively. Inhibition of histamine-induced bronchoconstriction was less marked, with PCf20 and PCs40 values of 0.19 (p greater than 0.05) and 0.21 (p less than 0.05) mg/ml. Thus, adenosine is a bronchoconstrictor in asthma whose effects are preferentially antagonized by concentrations of theophylline that cause little change in baseline airway caliber.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗

PubMed1985

The effects of acute bronchoconstriction on respiratory activity in patients with chronic obstructive pulmonary disease.

Attacks of acute airway obstruction often complicate the course of chronic obstructive pulmonary disease (COPD). In asthmatic subjects, bronchospasm triggers an increase in respiratory drive, which results in hyperventilation and hypocapnia. In the present study, we assessed the effects of acute bronchoconstriction induced by aerosolized methacholine on breathing and lung mechanics in 12 patients with stable COPD. Even low doses of methacholine markedly increased airway resistance and caused hyperinflation and decreased inspiratory muscle performance in the patients. Increasing airway obstruction produced a progressive rise in PCO2 despite an increase in minute ventilation. Breathing frequency and average inspiratory flow were greater, but tidal volume decreased because of shortening of the inspiratory duration. The magnitude of CO2 retention during acute bronchoconstriction was inversely related to the changes in tidal volume and inspiratory time (p less than 0.01 for each). In subjects with COPD, the occlusion pressure response to progressive hypercapnia failed to increase during bronchoconstriction. These results show that patients with COPD retain CO2 during acutely increasing airway obstruction induced by bronchoconstriction partly because of a rapid shallow breathing pattern that reduces alveolar ventilation.

Aged↗

PubMed1985

Adenosine-induced bronchoconstriction in asthma. Role of parasympathetic stimulation and adrenergic inhibition.

Adenosine by inhalation causes bronchoconstriction in asthmatic but not in normal subjects by an undefined mechanism. This study investigated the roles of cholinergic reflex stimulation and decreased beta 2-adrenoceptor responsiveness to explain adenosine's bronchoconstrictor action. The protection afforded by the inhaled muscarinic cholinergic antagonist, ipratropium bromide (IB) 1 mg, from bronchoconstriction induced by inhaled adenosine was compared with that of methacholine in 8 allergic asthmatic subjects. After saline placebo, the geometric mean concentrations of adenosine required to produce a 20% fall in FEV1 (PCf20) was 2.20 mg/ml and a 35% fall in SGaw (PCs35) was 1.97 mg/ml, which compared to 0.13 and 0.11 mg/ml, respectively, for methacholine. The IB increased FEV1 by 11 to 15% and SGaw by 69 to 73% and provided a large degree of protection against methacholine, with a geometric mean concentration ratio (CR) of 196 when airway caliber was measured as SGaw (p less than 0.001). In contrast, IB provided little protection against adenosine-induced bronchoconstriction (CR 1.3 for SGaw and 1.51 for FEV1). Beta 2-adrenoceptor responsiveness of the airways after inhaled adenosine and histamine was further studied in 12 asthmatic subjects by observing the antibronchoconstrictor effect of inhaled isoproterenol. After equivalent degrees of bronchoconstriction, 35 to 36% fall in FEV1 and 60 to 62% fall in SGaw cumulative doses of inhaled isoproterenol produced almost identical maximal increases in FEV1 and SGaw after adenosine as achieved after histamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗

PubMed1985

Differential inhibition of bronchoconstriction by the calcium channel blockers, verapamil and nifedipine.

Recent studies have demonstrated that the calcium channel blocking agents can inhibit experimentally induced bronchoconstriction in asthmatics, but their protective action has been variable. To clarify the influence of stimulus intensity and choice of calcium blocker on these reported differences in outcome, we performed noncumulative thermal stimulus-response curves using isocapnic hyperventilation of cold air in 8 asthmatics. Subjects received pretreatment with orally administered nifedipine (20 mg), intravenously administered verapamil (10 mg bolus followed by a continuous infusion), or appropriate placebos in a randomized, double-blind fashion. Verapamil afforded no consistent protection against the thermal challenges, whereas nifedipine significantly blunted the bronchoconstrictor response to stimuli of low (p less than 0.02) and middle (p less than 0.03) intensity. At the highest thermal burden, the effect of nifedipine was inconsistent and not significantly different from that of placebo. These results indicate that the protection from bronchoconstriction afforded by the calcium channel blockers depends on the choice of agent and the intensity of the bronchoconstricting stimulus, and they raise the possibility that the contribution of transmembrane calcium ion influx to the pathogenesis of bronchoconstriction may vary according to stimulus intensity.

Adult↗

PubMed1985

Homeostatic regulation of bronchomotor tone by sympathetic activation during bronchoconstriction in normal and asthmatic humans.

It has been assumed previously that the sympathetic nervous system (SNS) serves to antagonize bronchoconstrictor stimuli. To assess the homeostatic regulatory effect elicited by exogenously induced bronchoconstriction, we studied the effect of inhaled methacholine on the SNS response in 12 normal and 9 asthmatic humans. Exogenous SNS response was assessed as change in plasma epinephrine and norepinephrine concentrations from basal levels during inhalation challenge. A 74 +/- 3% decrease in specific airway conductance (SGaw) (p less than 0.001) was induced in normal subjects and a 78 +/- 7% decrease in asthmatics by methacholine challenge (p less than 0.001). Neither plasma epinephrine nor norepinephrine increased significantly from basal concentrations in normal or asthmatic subjects after maximal challenge (p greater than 0.33). To determine if physiologically achievable epinephrine concentrations potentially could modulate bronchoconstriction, the effect of intravenously infused epinephrine was measured in 11 of these subjects. After the highest dose of methacholine, a 15-min intravenous infusion of epinephrine (0.06 micrograms/kg/min) caused an 85 +/- 7% increase in SGaw in normal subjects (p less than 0.02). In asthmatics, a 319 +/- 68% increase in SGaw (p less than 0.002) was observed with similar changes in plasma epinephrine. Plasma epinephrine concentrations after infusion were comparable to those obtained in 4 normal and 1 asthmatic subject undergoing 60-degree, head-up tilt 1 h after volume depletion with intravenously administered furosemide. We conclude that physiologic concentrations of epinephrine can modulate moderately severe bronchoconstriction. However, the SNS does not regulate bronchomotor tone during mild to moderate bronchoconstriction.

Adolescent↗

PubMed2002

Acute protection against exercise-induced bronchoconstriction by formoterol, salmeterol and terbutaline.

The onset of bronchoprotection as obtained by various beta2-agonists has not been examined in a comparitive study. In this study, the onset of bronchodilation and protection against exercise-induced bronchoconstriction in asthmatics after inhalation of the long-acting beta2-agonists formoterol and salmeterol and the short-acting beta2-agonist terbutaline were measured. Twenty-five subjects with asthma and a history of exercise-induced bronchoconstriction (mean baseline forced expiratory volume in one second (FEV1): 90% predicted; mean fall in FEV1 after exercise: 31% from baseline) were enrolled in this double-blind, double-dummy, placebo-controlled, randomized, four-period crossover study. Exercise challenges were performed on 12 days at either 5, 30, or 60 min after inhalation of a single dose of formoterol (12 microg Turbuhaler), salmeterol (50 microg Diskus), terbutaline (500 microg Turbuhaler) or placebo. Exercise-induced bronchoconstriction (maximum fall in FEV1 or area under the curve) did not differ significantly between terbutaline, formorerol and salmeterol either 5, 30, or 60 min after inhalation of the study medication. In contrast, the onset of bronchodilation was slower after salmeterol compared to terbutaline and formoterol (p<0.05, each), which both showed a similar time course. At all time points between 5 and 60 min, formoterol provided significantly greater bronchodilation than salmeterol (p<0.05). These data indicate that equipotent doses of the bronchodilators salmeterol, formoterol and terbutaline were similarly effective with respect to their short-term protective potency against exercise-induced bronchoconstriction, despite the fact that the time course of bronchodilation was significantly different between the three beta2-agonists.

Administration, Inhalation↗

PubMed1996

Effect of the 21-aminosteroid U-74006F on antigen-induced bronchoconstriction and bronchoalveolar eosinophilia in allergic sheep.

U-74006F, a non-glucocorticoid 21-aminosteroid, has been developed as an inhibitor of iron-dependent lipid peroxidation. This class of compounds has been shown to prevent antigen-induced eosinophil accumulation in the lungs. In this study, Ascaris-sensitive, "dual-respondent" sheep (showing both immediate (IAR) and late (LAR) asthmatic response) (n = 6) were used to assess the effect of U-74006F on antigen-induced bronchoconstriction and airway inflammation and reactivity 8 h after antigen challenge. Antigen provocation induced dual-phase bronchoconstriction, bronchoalveolar eosinophilia and airway hyperreactivity (AHR) to methacholine. Throughout the experiment, intravenous administration of the drug significantly reduced the IAR and inhibited the LAR along with the inhibition of eosinophil influx, but did not inhibit the increase in airway reactivity observed 8 h after antigen challenge. Post-antigen challenge treatment with U-74006 from 3 h after antigen challenge also significantly reduced the LAR and bronchoalveolar eosinophilia, although the degree of inhibitory effect was milder. The development of the LAR appeared to be dependent on eosinophil recruitment into the lungs. These findings suggest that lipid peroxidation is involved in antigen-induced bronchoconstriction and eosinophil recruitment into the lungs, and that the inhibitor U-74006F may be an effective drug for the treatment of bronchoconstriction and airway inflammation characterized by eosinophil infiltration in asthmatics.

Allergens↗

PubMed1975

The role of bronchoconstriction in cough reflex.

To investigate the role of bronchoconstriction in the cough reflex, we compared antitussive effects of several drugs with their ability to effect the respiratory tract (i.e. bronchodilation vs. bronchoconstriction). Antitussive activities of five drugs administered either intravenously or orally on electrically-induced cough were evaluated in the non-anesthetized dog. The antitussive activities were as follows: morphine, 0.1 mg/kg (i.v.) and 0.5 mg/kg (p.o.); codeine, 1.0, 4.0; picoperidamine, 2.0, 9.8; piclobetol, 7.6, 9.0; HH-197, 12.5, 143.0, respectively. Morphine, codeine and HH-197 caused bronchoconstriction, but picoperidamine and picrobetol caused bronchodilation. The antitussive and bronchodilatation effects of isoproterenol were abolished by propranolol. Each bronchoconstricting drug (i.e. morphine, codeine and HH-197) was administered concurrently with isoproterenol (10 mug/kg, i.v., and non-antitussive activity), and the cough reflex was observed. Compared with the single administration of each drug, respiratory resistance was decreased and the antitussive effect was increased. These results indicate a strong correlation between bronchodilatation and increased antitussive activity.

Airway Resistance↗

PubMed1987

The effect of trans-4-guanidinomethylcyclohexanecarboxylic acid p-tert-butylphenyl ester hydrochloride (NCO-650) on Ascaris suum antigen-induced bronchoconstriction in dogs.

Antiallergic asthma effect of trans-4-guanidinomethylcyclohexane-carboxylic acid p-tert-butylphenyl ester hydrochloride (NCO-650), a new anti-allergic drug, was investigated in comparison with those of tranilast and disodium cromoglycate (DSCG) in anesthetized dogs. The asthmatic bronchoconstriction was induced by inhalation of Ascaris suum antigen (Asc-Ag) to naturally Ascaris-sensitive dogs. The airway resistance was determined using the modified Konzett-Rössler method. Both intravenous (1 and 5 mg/kg) and intraduodenal (10, 30 and 100 mg/kg) administrations of NCO-650 prior to the antigen challenge markedly inhibited the asthmatic bronchoconstriction induced by Asc-Ag inhalation. The antiasthmatic effect of NCO-650 was much stronger than that of DSCG (10 mg/kg, i.v.) and was about three-fold stronger than that of tranilast. On the other hand, when NCO-650 was administered after the antigen challenge, the agent had no inhibitory effect on the Asc-Ag induced bronchoconstriction. As for the effects on increased airway secretion at the time of asthmatic attack, NCO-650 inhibited the excessive secretions without any remarkable change in the viscosity of the secretions. NCO-650 had no effect on the bronchoconstriction induced by inhalation of acetylcholine, suggesting that NCO-650 appears to have no anti-cholinergic effect and thus no effect on the vagal reflex that occurred during the asthmatic responses. The above findings show that NCO-650 may be useful for the treatment of bronchial asthma as an orally active drug.

Acetylcholine↗

PubMed1990

Inhibitory effects of OKY-046 on spasmogen-induced bronchoconstrictions in sensitized and non-sensitized guinea pigs.

We examined the effect of thromboxane A2 (TXA2) synthetase inhibitor, OKY-046, on bronchoconstriction induced by antigen and various spasmogenic mediators in guinea pigs in vivo. Further, inhibitory activities of OKY-046 on contractions of isolated tracheae and lung parenchymal strips induced by various contractile agents were also investigated in vitro. OKY-046, but not indomethacin, significantly inhibited antigen-induced bronchoconstriction in a dose-dependent manner. Moreover, OKY-046 attenuated bronchoconstrictions induced by peptide leukotrienes (LTs) and platelet activating factor (PAF), but not those by histamine, prostaglandin D2 (PGD2) and STA2 (a stable TXA2 mimetic agent). Although contractile responses induced by spasmogens such as peptide LTs, PAF and histamine were not influenced by OKY-046 in isolated tracheae, OKY-046 elicited significant and concentration-dependent inhibitions against contractile responses induced by peptide LTs and PAF in isolated lung parenchymal strips. These results suggest the possible involvement of TXA2 in the development of anaphylactic bronchoconstriction in sensitized guinea pigs.

Acrylates↗

PubMed1985

Comparative modification of antigen-induced bronchoconstriction by the calcium antagonists, nifedipine and verapamil.

We compared the effects of the two calcium antagonists, nifedipine and verapamil, on baseline airway function and antigen-induced bronchoconstriction in asymptomatic subjects with ragweed hypersensitivity and a history of bronchial asthma. Twelve subjects received a single oral dose of 20 mg of nifedipine or 160 mg of verapamil before inhalation with ragweed antigen. Mean specific airway conductance, a measurement of airway obstruction, was not affected by either agent; nifedipine caused bronchodilatation in two subjects, and verapamil was followed by slight bronchoconstriction in another subject. Nifedipine partially or completely blocked the antigen-induced bronchoconstriction in 67 percent (8/12) of the subjects (p less than 0.05). Two of the subjects who were protected by nifedipine were also protected by pretreatment with verapamil, while this drug was without effect in the others. This study demonstrates that both nifedipine and verapamil in a single oral dose may attenuate antigen-induced bronchoconstriction in some subjects with allergic bronchial asthma and that nifedipine may be more effective than verapamil.

Adult↗

PubMed1983

The effect of adrenergic and cholinergic drugs on methacholine- and histamine-induced bronchoconstriction in monkeys.

The effect of adrenergic and cholinergic drugs on bronchial contraction of monkeys was studied using bronchoconstriction induced by aerosol challenge with methacholine and histamine. Under the anesthesia with ketamine hydrochloride, changes in the total respiratory resistance were continuously measured in monkeys to estimate the bronchial response to both histamine and methacholine. Isoprenaline decreased bronchial susceptibility to aerosol challenge with both methacholine and histamine. Isoprenaline was also potent in antagonizing the bronchoconstriction induced by methacholine and histamine. Atropine decreased bronchial susceptibility to aerosol challenge with methacholine and also partially with histamine. Atropine also antagonized the bronchoconstriction induced by methacholine, but not by histamine. Phentolamine had neither inhibitory effects on the aerosol challenge with methacholine and histamine, nor produced an antagonistic effect on bronchoconstriction induced with methacholine and histamine.

Animals↗

PubMed1989

Individual differences in regional deposition of 6-micron particles in humans with induced bronchoconstriction.

The effect of induced bronchoconstriction on regional lung deposition of 6 microns aerodynamic diameter 99mTc-labeled Teflon particles was studied in eight healthy non-smokers. The Teflon particles were inhaled at 0.5 l/s from a 25-l glass bulb with 8-12 maximally deep breaths on four consecutive days. For three exposures, various degrees of bronchoconstriction were induced using an aerosol of methacholine bromide before the inhalation of the Teflon particles. For the fourth (control) exposure, bronchoconstriction was induced after the inhalation of the Teflon particles. The degree of bronchoconstriction was quantified by measurements of airway resistance (Raw) using a whole-body plethysmograph. The fraction of alveolarly deposited particles in the lung (FAD) was estimated by measurements of radioactivity in the lung immediately after inhalation of the Teflon particles and 6 h later. Earlier studies have shown that when the mucociliary transport is stimulated with the cholinergic aerosol used in this study, the 6-h retention values (Ret6) are similar to the 24-h values. Within the subjects there was a close relationship between Raw and Ret6 with a decrease of Ret6 with increased Raw. This decrease varied markedly among the subjects. The relationship between Raw and Ret6 calculated from the model by the Task Group on Lung Dynamics, in which the airway diameters were varied, agreed with our experimental data. On an average, airway resistance of 1 and 2 cm H2O.s/l correspond to FAD of about 50% and 25%, respectively.

Administration, Inhalation↗