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PubMed1978

An investigation of the mechanism of ethanol-induced bronchoconstriction.

A 28-year-old Asian-American woman complained of symptoms of acute bronchoconstriction after drinking alcohol beverages. We documented the presence of ethanol-induced bronchoconstriction in this patient by administering oral ethanol challenges under controlled conditions. Bronchoconstriction was not prevented by pretreatment with atropine sulfate or cromolyn, suggesting that neither cholinergic postganglionic pathways nor mediator release from mast cells was the cause of the acute airway narrowing. The rapid decrease in specific airway conductance after ethanol ingestion and the association with symptoms of vasomotor sensitivity suggest that ethanol may have acted in this patient by releasing one or more secondary mediators with vasoactive and bronchoactive properties.

Adult↗

PubMed1986

Etiopathogenic mechanisms of bronchoconstriction in byssinois--a review.

Studies of etiopathogenic mechanisms of bronchoconstriction in byssinosis indicate the possible involvement of histamine, 5-HT, platelet-activating factor, and metabolites of arachidonic acid as mediators of bronchoconstriction. These substances might be released by a variety of lung and/or recruited cells to induce construction of respiratory airways characteristic of the acute byssinotic reaction. It certainly seems possible that cotton dust induces acute bronchoconstriction by more than one mechanism and that a number of factors, both endogenous and exogenous, influence the increased bronchomotor response to cotton dust inhalation in any given textile worker.

Airway Resistance↗

PubMed1987

Bradykinin-induced bronchoconstriction in humans. Mode of action.

The effect of bradykinin was studied by inhalation in normal and asthmatic human subjects, as well as on human bronchial smooth muscle in vitro. Bradykinin caused cough and retrosternal discomfort in all subjects and bronchoconstriction in asthmatic subjects. Bradykinin was approximately 10 times more potent than histamine and methacholine, and there was a significant correlation between the subjects' sensitivity to histamine and bradykinin. Bradykinin-induced bronchoconstriction was prolonged when compared with that of histamine and the C-fiber stimulant capsaicin. This bronchoconstriction was subject to tachyphylaxis, which was also associated with desensitization of the subjects to inhaled histamine. The provocative dose causing a 35% fall in specific airway conductance (PD35) was unaffected by aspirin (1 g orally). However, ipratropium bromide (0.25 mg by nebulizer) significantly inhibited the effect of bradykinin, the PD35 being 0.8 mumol (range, 0.16 to 3.4) and 0.15 mumol (range, 0.047 to 1.15) after active dose and placebo, respectively (p less than 0.05). Likewise, cromolyn sodium (40 mg dry powder) also significantly reduced response to bradykinin, with a PD35 of 0.04 mumol (range, 0.13 to 0.31) after placebo and 0.39 mumol (range, 0.05 to 4.45) after SCG (p less than 0.05). Bradykinin only weakly constricted human bronchial smooth muscle in vitro. Bradykinin at 10(-4) caused only 21.5 +/- 5.5% of the maximal carbamylcholine contraction in 11 of 18 airways. Captopril did not enhance the effect of bradykinin. Bradykinin is a potent bronchoconstrictor of human airways in vivo, acting in part through cholinergic mechanisms but not because of the formation of prostaglandins.

Administration, Inhalation↗

PubMed2001

Nedocromil sodium versus sodium cromoglycate in treatment of exercise-induced bronchoconstriction: a systematic review.

The objective of this review was to compare the effects of prophylactic doses of nedocromil sodium (NCS) and sodium cromoglycate (SCG) on postexercise lung function, in persons diagnosed with exercise-induced bronchoconstriction. Randomized controlled trials were identified from the Cochrane Airways Review Group Asthma Register, plus hand searching for trials in journals, bibliographies of relevant studies and review articles. Randomized controlled trials comparing NCS to SCG in prophylactic treatment of exercise-induced bronchoconstriction were eligible. Studies were pooled using odds ratios (OR) for dichotomous outcomes or weighted mean differences (WMD) with 95% confidence intervals (95% CI) for continuous outcomes. No significant differences were noted between NCS and SCG with respect to the maximum per cent decrease in forced expiratory volume in one second (WMD=-0.88; 95% CI -4.50-2.74), complete protection (OR=0.95; 95% CI 0.50-1.81), clinical protection (OR=0.71; 95% CI 0.36-1.39), unpleasant taste (OR=6.85; 95% CI 0.77-60.73), or sore throat (OR=3.46; 95% CI 0.32-37.48). Subgroup analyses based on age, dosages of medications and timing of exercise postinhalation were consistent with the overall pooled analyses. No significant differences were evident between the effects of nedocromil sodium and sodium cromoglycate during the immediate postexercise period in adults and children with exercise-induced bronchoconstriction, with regards to maximum per cent decrease in forced expiratory volume in one second, complete protection, or clinical protection. Side-effect profiles were similar.

Adult↗

PubMed2005

Adenosine level in exhaled breath increases during exercise-induced bronchoconstriction.

In asthmatic patients, airway obstruction provoked by exercise challenge is accompanied by an increase in plasma adenosine level. In this study, the current authors investigated if exercise-induced bronchoconstriction was associated with local changes of adenosine concentration in the airways. Oral exhaled breath condensate (EBC) collection (5-min duration) and forced expiratory volume in one second (FEV1) measurements were performed at rest (baseline) and 4-8 times after treadmill exercise challenge in healthy and asthmatic subjects. Adenosine concentration in EBC was determined by HPLC. Observations indicated that physical exercise results in bronchoconstriction together with a significant increase of adenosine level in EBC in asthmatic patients (mean+/-sd maximal fall in FEV1 27+/-13%; associated increase in adenosine 110+/-76% as compared to baseline), but not in healthy control subjects. Exercise-induced changes in adenosine concentration correlated significantly with the fall in FEV1 values in asthmatic patients. In conclusion, the observed increase in adenosine concentration of oral exhaled breath condensate most probably reflects changes in the airways during exercise-induced bronchoconstriction. Due to its known bronchoconstrictor property in asthma, adenosine may contribute to the development of bronchospasm.

Adenosine↗

PubMed1996

Changes in respiratory drive account for the magnitude of dyspnoea during bronchoconstriction in asthmatics.

To evaluate whether the interindividual differences in dyspnoea perceived by asthmatic subjects for the same level of airway narrowing could depend on different changes in respiratory drive, we assessed the relationship between changes in airway calibre, changes in neuromuscular output, and dyspnoea rate during progressive bronchoconstriction induced by methacholine. We studied 18 asymptomatic asthmatic subjects (aged 18-36 yrs; 11 males and 7 females) with normal lung function. Dyspnoea (Borg scale), mouth occlusion pressure (P0.1), and forced expiratory volume in one second (FEV1) were measured at baseline and after inhalation of aerosols of doubling concentrations of methacholine (MCh). The progressive bronchoconstriction induced by MCh was associated with a progressive increase both of P0.1 and dyspnoea. Dyspnoea score was linearly related either to the fall in FEV1, or to the increase in P0.1. However, the slope values of the relationship between dyspnoea score and the corresponding percent fall in FEV1 showed a large interindividual variability (0.05-0.32; coefficient of variability (CoV) 43%). By contrast, the slope values of the relationship between dyspnoea score and the corresponding percent increase in P0.1 ranged 0.02-0.05 (CoV = 14%), indicating a more homogeneous response to dyspnoea for the same change in P0.1. At the highest MCh concentration, the dyspnoea score was linearly related to the corresponding change in P0.1 (r = 0.91; p < 0.01), but not to the corresponding percentage fall in FEV1 (r = 0.28). These results show that the interindividual differences in dyspnoea perceived by asthmatic subjects for the same level of airway narrowing are associated with different changes in respiratory drive during bronchoconstriction.

Adolescent↗

PubMed1990

The effect of substance P on the antigen-induced bronchoconstriction in guinea pigs.

The effect of substance P (SP) on the antigen-induced bronchoconstriction in vitro and in vivo was investigated in guinea pigs. SP caused the contraction of isolated non-sensitized guinea pig tracheal muscle at concentrations between 10(-9) to 10(-7) g/ml. The elimination of epithelium in the tracheal muscle produced a slight enhancement of SP response as compared to control. Antigen-induced contraction of isolated sensitized guinea pig tracheal muscle was slightly enhanced by the pretreatment with SP at a concentration of 10(-9) g/ml. The SP-induced enhancement of antigen-induced contraction was significantly augmented by the elimination of epithelium of sensitized tracheal muscle. Moreover, the clear bronchoconstriction was observed by the infusion of SP (1 micrograms/min) intravenously, but not by the infusion of SP at the rates between 0.1 and 0.01 micrograms/min. Antigen-induced asthmatic respiratory disorder was accelerated temporarily by the infusion of subthreshold SP (0.1 microgram/min). The reactivity of bronchial smooth muscle measured by repeated injection of acetylcholine was significantly potentiated by the infusion of subthreshold SP (0.1 microgram/min). These results suggest that SP has dual actions in the contractile response of guinea pig airway smooth muscle. One is the direct contractile activity, and the other one is enhancing activity of antigen- and acetylcholine-induced bronchoconstriction.

Airway Resistance↗

PubMed1979

Effects of breathing warm humidified air on bronchoconstriction induced by body cooling and by inhalation of methacholine.

The effect of breathing warm humidified air upon bronchoconstriction induced with body cooling or inhalation of methacholine was studied in two groups of eight asthmatic subjects. One group had the body cooled using one-minute exposures, first to a cold shower at 15 degrees C and then to a current of wind. The other group received methacholine by inhalation until a decrease of 20 percent or more occurred in the forced expiratory volume in one second. Both groups of asthmatic subjects were tested when breathing room air and warm humidified air. Pulmonary functions were assessed before and after cooling of the body and during inhalation of methacholine. Breathing warm humidified air substantially reduced bronchoconstriction induced by body cooling, but not that induced by inhalation of methacholine. Thus, bronchoconstriction induced by cooling of the body appears to be related to cooling of the airways, which may be compensated by breathing warm humidified air.

Airway Resistance↗

PubMed1981

Atropine and exercise-induced bronchoconstriction.

Six asthmatic children were studied to determine whether supplemental, parenteral atropine would increase the effects of bronchodilation and protection against exercise-induced bronchoconstriction after maximal effects had been achieved by inhalation. First, we determined the amount of inhaled atropine sulfate that would give maximal bronchodilation for each patient at rest. This quantity of atropine was designated as "A." Then all subjects exercised for five sessions with the following pre-exercise treatments in a random order: (a) inhaled distilled water plus intramuscular (IM) saline solution; (b) inhaled A dose of atropine plus IM saline solution; (c) inhaled distilled water plus 0.35 mg IM atropine; (d) inhaled A dose of atropine plus 0.35 mg IM atropine; and (e) inhaled double the A dose plus IM saline solution. The results showed that the combination of inhaled and IM atropine had the greatest bronchodilation effect and the greatest protection against exercise-induced bronchoconstriction. Atropine inhalation alone (A dose) or IM injection (0.35 mg) was not as effective in bronchodilation or in alleviation of exercise-induced bronchoconstriction. Doubling the dose of inhalation (2A) did not increase the effects of the A dose. These results support the hypothesis that inhaled atropine does not reach all the airways where cholinergic receptors are present.

Adolescent↗

PubMed1989

Lidocaine-induced bronchoconstriction in asthmatic patients. Relation to histamine airway responsiveness and effect of preservative.

Inhaled topical lidocaine, used to produce anesthesia of the respiratory tract prior to bronchoscopy, may cause bronchoconstriction in asthmatic patients. We investigated whether the degree of histamine airway responsiveness would predict the development and extent of lidocaine-induced bronchoconstriction in 20 asthmatic patients. The provocation concentration of histamine producing a 20 percent fall in FEV1 (PC20) was measured. On a separate day, challenge with 6 ml 4 percent lidocaine (Xylocaine 4 percent topical) was performed. There was no correlation between the response to lidocaine and the histamine PC20. Five patients (25 percent) showed a fall in FEV1 of greater than 15 percent (max 42.1 percent). Three responders were rechallenged double-blind with the commercial 4 percent lidocaine preparation and with a 4 percent preservative-free lidocaine solution. There was no difference in the response to these two solutions. These results demonstrate that inhaled topical lidocaine induces bronchoconstriction in a significant proportion of patients with asthma. This response is not related to airway histamine responsiveness or to the preservative in the lidocaine preparation.

Administration, Inhalation↗

PubMed1990

Airways responses to ipratropium bromide do not vary with time in asthmatic subjects. Studies of interindividual and intraindividual variation of bronchodilatation and protection against histamine-induced bronchoconstriction.

Bronchial histamine provocation tests were performed in nine patients with nonallergic asthma on four consecutive days 45 minutes after inhalation of placebo or ipratropium bromide in a dose-response manner (40 micrograms, 200 micrograms, and 800 micrograms). The drugs were administered double-blind, one dose on each day. This procedure was repeated identically after three to nine months to investigate whether the bronchial responses to ipratropium bromide are constant or change with time. Ipratropium bromide induced a significantly better bronchodilation and protection against histamine-induced bronchoconstriction than placebo with no differences between the three doses. No correlation between bronchodilatation and protection was found. In six asthmatic patients ("responders") ipratropium bromide induced a significant protective effect against histamine-induced bronchoconstriction but no dose-response relationship was found. In three patients none or a very poor protective effect was found at all dose levels ("nonresponders"). The protective effect of ipratropium bromide against histamine-induced bronchoconstriction did not differ between the first and second occasion. Thus, the bronchoprotection differed between different asthmatic subjects but did not vary with time (three to nine months) within the same subject. This finding seems to be of clinical importance since it implicates that the effect of anticholinergic agents on the airways is predictable.

Administration, Inhalation↗

PubMed1989

Effect of nedocromil sodium on bronchoconstriction induced by adenosine and tachykinins.

Purines and neuropeptides may act as neurotransmitters of the local axon reflex in the airways. Nedocromil sodium has been shown to inhibit adenosine- and neurokinin A-induced bronchoconstriction both in the rat and in man. In this study we used the rat model for further investigation of the mechanism of action of nedocromil sodium in the adenosine- and neurokinin A-challenge. The animals were challenged intravenously, and immediately after maximal bronchoconstriction a bronchoalveolar lavage was performed and histamine was assayed in the supernatant of the lavage fluid. Nedocromil sodium significantly inhibited the adenosine- and the neurokinin A-induced increase in histamine concentration in the lavage fluid. Nedocromil sodium had no influence on the airway responsiveness to serotonin or carbachol. We therefore concluded that the inhibitory effect of nedocromil sodium on adenosine- and neurokinin A-induced bronchoconstriction can be explained by its activity on airway mast cells.

Adenosine↗

PubMed1987

Ipratropium bromide: bronchodilator action and effect on methacholine-induced bronchoconstriction.

The effects of ipratropium bromide (80 and 200 micrograms) and placebo on the basal bronchial tone and on methacholine-induced bronchoconstriction were investigated in 10 asthmatic patients in a placebo-controlled double-blind manner. Bronchial hyperreactivity to methacholine was confirmed at a pretrial bronchial challenge. The patients were randomly allocated to two groups in which the drug was inhaled from either metered-dose inhalers (MDI) or powder capsules. With the high dosage, the bronchodilation resulting from powder capsules was somewhat more pronounced than that achieved with the MDI. Otherwise the bronchodilator effect of ipratropium bromide and the protection afforded by the drug against methacholine-induced bronchoconstriction were similar in the two groups. In five patients the bronchodilator effect was better and in four patients the tolerance to methacholine was greater after the higher ipratropium dosage than after the lower one. In two patients ipratropium bromide had no bronchodilator effect but gave good protection against methacholine-induced bronchoconstriction. It is concluded that some patients benefit from a dosage of ipratropium bromide higher than that usually recommended and that an anticholinergic effect on the bronchi is possible even in the absence of the bronchodilator effect in the basal state.

Administration, Inhalation↗

PubMed1975

The correlation between exercise-induced bronchoconstriction and bronchial methacholine sensitivity in asthma.

A possible relationship between exercise-induced bronchoconstriction (EIB) and bronchial sensitivity to the cholinergic drug, metacholine, was studied. On the same day, 57 asthmatic subjects inhaled increasing concentrations of the drug and were then tested for EIB by exercising to exhaustion. A fall in peak expiratory flow rate of 15% or more was considered a positive reaction to either test. Of the 45 patients exhibiting a positive methacholine reaction, 33 showed bronchoconstriction after exercise (including three of the ten who had no previous history of exertional asthma) while none of the 12 methacholine nonreactors developed EIB. This significant correlation (P is less than .001) between the tendency to develop EIB and sensitivity to methacholine suggests that bronchoconstriction, induced either by exercise or methacholine, is a specific reaction.

Adolescent↗

PubMed1990

Airway opioid receptors mediate inhibition of cough and reflex bronchoconstriction in guinea pigs.

Effects of opioids and opioid antagonists on citric acid-induced cough and reflex bronchoconstriction have been examined in conscious guinea pigs. Airway reflexes produced by inhaled citric acid are mediated by capsaicin sensitive sensory neurons, and we examined particularly the possibility that inhibitory effects of opioids can be exerted locally in the airway. As expected, systemically administered codeine (1-10 mg/kg), meperidine (3-30 mg/kg) and morphine (1-10 mg/kg) dose-dependently inhibited cough and bronchoconstriction. However, inhalations of nebulized codeine (10-100 mg/ml) and morphine (10-30 mg/ml) also produced these effects. The potency and rapid onset of action of inhaled codeine suggest that it exerted its effects without first being metabolized to morphine. The opioid receptor antagonist naloxone completely (10-100 micrograms/kg), and nalorphine (a mixed agonist/antagonist) (1-3 mg/kg) partly, inhibited codeine's antitussive and antibronchoconstrictor effects. Nalorphine alone (3-30 mg/kg) inhibited citric acid induced reflexes, whereas naloxone was without effect. Prior inhalation of a quaternary opioid receptor antagonist, levallorphan methyl iodide (10 mg/ml), abolished the inhibitory effects of inhaled codeine (30 mg/ml). The present data suggest that inhibition of cough and reflex bronchoconstriction can be produced by opioids, acting on mu and kappa receptors located in the guinea pig tracheobronchial tree. The possible existence in the airways of a unique opioid receptor mediating inhibition of cough (as described in the central nervous system) cannot be excluded.

Animals↗

PubMed1990

The prevalence of exercise-induced bronchoconstriction in Cape Town schoolchildren.

An attempt was made to determine: (i) the prevalence of exercise-induced bronchoconstriction among white and coloured schoolchildren in Cape Town; and (ii) the validity of an exercise test for the diagnosis of asthma in the general population. Children (698 white and 494 coloured) were randomly drawn from schools in the northern suburbs of Cape Town. Each child participated in a standard 6-minute exercise test and spirometric measurements were taken before and 10 minutes after exercise with a portable spirometer. The diagnosis of asthma was based on a questionnaire and personal questioning and included those children who, in the past or at present, suffered episodic or continuous airflow obstruction, which was responsive to a bronchodilator. The criterion for the diagnosis of exercise-induced bronchoconstriction was a 10% decline in forced expiratory volume in 1 second after exercise. The prevalence of exercise-induced bronchoconstriction was significantly higher among white children (5.87%) than coloured children (4.05%). The sensitivity of the exercise test was 0.31 and the specificity 0.97. In contrast to the results of hospital-based studies, the negative predictive value of an exercise test (95%) was found to be greater than the positive predictive value (46%). It is therefore concluded that exercise testing is not a useful screening test for epidemiological use; it is probably useful as a challenge test for detecting asthma in the individual patient when the likelihood of the disease is high.

Adolescent↗

PubMed1989

[Inhalation of a precursor analogue of vasoactive intestinal polypeptide (Leu17 VIP-Gly-Lys) protects ascaris-induced bronchoconstriction in dog].

We studied in vivo the effects of pre-inhalations of vasoactive intestinal polypeptide (VIP) and a precursor analogue of VIP (Leu17 VIP-Gly-Lys: preVIP) in mongrel dogs bronchoconstricted by ascaris. An inhalation of preVIP solution (2 mg/5 ml saline) gave significant protection for 120 min against increases in respiratory resistance (Rrs) and decreases in dynamic compliance (Cdyn) induced by ascaris challenges. An inhalation of VIP solution (2 mg/ml saline) also gave significant protection for 120 min against increases in Rrs induced by ascaris challenges. Protective effect of the inhalation of preVIP against ascaris-induced bronchoconstriction was more potent than that of VIP. The inhalations of preVIP and VIP solution did not change systemic blood pressure or heart rate. These results indicate that inhalations of preVIP or VIP solution would attenuate ascaris-induced bronchoconstriction in dogs without affecting cardiovascular dynamics.

Administration, Inhalation↗

PubMed1989

Comparison of the constant flow and occlusion methods for assessment of bronchoconstriction in guinea-pigs.

Assessments of total respiratory compliance (C) and conductance (G) with the constant inspiratory flow and the occlusion methods were compared in the basal state and during histamine or serotonin induced bronchoconstriction in 22 normal, anaesthetized, paralysed, mechanically ventilated guinea-pigs. In the basal state, no significant difference was found between the C and G values measured by both methods. During drug-induced bronchoconstriction, small but significant differences were observed between the respiratory parameters measured by the two methods, and expressed as the percentage ratio (R) to the corresponding basal values (respectively RCCF and RCOC, and RGCF and RGOC). This discrepancy, which was independent of the drug and of the dose, was probably attributable to a modification of the visco elastic properties of the lung due to either the mechanical ventilation or the infused drug. Nevertheless, this study demonstrates that both methods can be considered as equivalent for bronchoconstriction assessment because very strong correlations were found between RCCF and RCOC (r = 0.96, p less than 0.001) and between RGCF and RGOC (r = 0.97, p less than 0.001), and because the slopes of the linear relationships were not significantly different from unity in both cases.

Animals↗