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PubMed2005

Bronchoconstriction provoked by exercise in a high-particulate-matter environment is attenuated by montelukast.

Airborne ultrafine and fine particulate matter (PM1 from fossil-fueled internal combustion engines may cause abnormal airway narrowing. Because of high PM1 exposure from ice resurfacing machines, the ice-rink athlete is especially vulnerable to PM1 toxicity. The purpose of this study was to evaluate protection by a single dose of montelukast in college ice hockey players following PM1 exposure exercise. Nine male ice hockey players (age 19.3+/-1.22 yr) performed 4 randomized, double-blinded, high-intensity, 6-min cycle ergometer trials in low [PM1] (2260+/-500 particles/cm3) and high [PM1] (348,600+/-121,600 particles/cm3) after placebo or montelukast. Pre- and postspirometry showed similar peak FEV1 (forced expiratory volume in 1 s) falls between placebo and montelukast after low [PM1] trials (14.5+/-18.06 vs. 9.5+/-11.75% of baseline, respectively). Peak FEV1 falls after high [PM1] trials were greater for placebo than for montelukast (17.3+/-9.79% vs. 1.7+/-5.77% of baseline; p<.0001). High [PM1] FEV1 fall after exercise following montelukast ingestion was less than after exercise following placebo ingestion under high and low [PM1] conditions and after exercise following montelukast ingestion under low [PM1] conditions at 5, 10, and 15 min postchallenge (p<.004, .0006, .009, respectively). Montelukast provided greater protection against bronchoconstriction after exercise during high [PM1] than low [PM1] exposure (approximately 90% vs. approximately 35%), suggesting that bronchoconstriction from PM1 exposure is predominately leukotriene mediated. The precise mechanism of airborne PM1-induced leukotriene-mediated airway narrowing remains unclear.

Acetates↗

PubMed2001

Effects of unilateral bronchoconstriction on distribution of aerosols in ovine airways.

The purpose of the study was to assess the effect of unilateral bronchoconstriction on the deposition patterns of aerosolized particles in a sheep model. Unilateral bronchoconstriction was induced in intubated conscious sheep by placing a protective, obstructing balloon catheter in either main bronchus, prior to administration of aerosolized carbachol at a dose that increased pulmonary resistance by 200-400% above baseline. The catheter was then removed and the animals were positioned under a gamma camera. An equilibrium image was obtained with xenon (133Xe), to determine a lung outline that was used to calculate the proportion of counts in each lung. Aerosols, labeled with technetium (99mTc) and generated by two jet nebulizers, were inhaled tidally by the sheep in serial experiments. (For nebulizer A, mass median aerodynamic diameter [MMAD] = 0.39 microm; for nebulizer B, MMAD = 1.1 microm.) For nebulizer A, percentage deposition in the treated and untreated lungs was not significantly different (50.8% versus 49.2%, respectively), while for nebulizer B, the median deposition in the carbachol treated lung was significantly greater than in the untreated lung (55.8% versus 44.2% respectively; p = 0.005). There was a more central pattern of deposition in the treated lung than in the untreated lung for both nebulizers, but the degree of central deposition was significantly greater with nebulizer B. The findings of the present study suggest that regional obstruction does not preclude the delivery of therapeutic aerosols to the airways in such a region, and may, depending on the size of the aerosol, result in enhanced airway deposition relative to less obstructed regions.

Aerosols↗

PubMed1999

Endotracheal intubation, but not laryngeal mask airway insertion, produces reversible bronchoconstriction.

BACKGROUND: Tracheal intubation frequently results in an increase in respiratory system resistance that can be reversed by inhaled bronchodilators. The authors hypothesized that insertion of a laryngeal mask airway would be less likely to result in reversible bronchoconstriction than would insertion of an endotracheal tube. METHODS: Fifty-two (45 men, 7 women) patients were randomized to receive a 7.5-mm (women) or 8-mm (men) endotracheal tube or a No. 4 (women) or No. 5 (men) laryngeal mask airway. Anesthesia was induced with 2 microg/kg fentanyl and 5 mg/kg thiopental, and airway placement was facilitated with 1 mg/kg succinylcholine. When a seal to more than 20 cm water was verified, respiratory system resistance was measured immediately after airway placement. Inhalation anesthesia was begun with isoflurane to achieve an end-tidal concentration of 1% for 10 min. Respiratory system resistance was measured again during identical conditions. RESULTS: Among patients receiving laryngeal mask airways, the initial respiratory system resistance was significantly less than among patients with endotracheal tubes (9.2+/-3.3 cm water x 1(-1) x s(-1) [mean +/- SD] compared with 13.4+/-9.6 cm water x 1(-1) x s(-1); P < 0.05). After 10 min of isoflurane, the resistance decreased to 8.6+/-3.6 cm water x 1(-1) x s(-1) in the endotracheal tube group but remained unchanged at 9.1+/-3.3 cm water x 1(-1) x s(-1) in the laryngeal mask airway group. The decrease in respiratory system resistance in the endotracheal tube group of 4.7+/-7 cm water x 1(-1) x s(-1) was highly significant compared with the lack of change in the laryngeal mask airway group (P < 0.01). CONCLUSIONS: Resistance decreased rapidly only in patients with endotracheal tubes after they received isoflurane, a potent bronchodilator, suggesting that reversible bronchoconstriction was present in patients with endotracheal tubes but not in those with laryngeal mask airways. A laryngeal mask airway is a better choice of airway to minimize airway reaction.

Anesthesia↗

PubMed1999

Relaxant effect of magnesium and zinc on histamine-induced bronchoconstriction in dogs.

OBJECTIVE: Magnesium sulfate (MgSO4) has been reported to produce bronchodilation in asthmatic patients. In vitro studies have suggested that divalent cations inhibit L-type voltage-sensitive calcium ion (Ca2+) channels in cardiac and smooth muscles. In this study, we evaluated the in vitro and in vivo effects of magnesium ion (Mg2+) and zinc ion (Zn2+) on the airway contracted by histamine. SETTING: A university research laboratory. SUBJECTS IN VITRO: Tracheal smooth muscle from guinea pigs. IN VIVO: Mongrel dogs. MEASUREMENTS AND MAIN RESULTS IN VITRO STUDY: The tension of isolated guinea pig tracheal strips was measured isometrically with a force displacement transducer. The specimen was contracted with histamine (10 microM). Then, MgSO4 (n = 6), zinc sulfate (ZnSO4, n = 6), or sodium sulfate (Na2SO4, n = 6) was cumulatively added to the organ bath. IN VIVO STUDY: The bronchial cross-sectional area of mongrel dogs was measured by a direct visualization method demonstrated previously. The dogs were randomly assigned to three groups: group Mg (n = 7), group Zn (n = 7), and group Na (n = 7). Bronchoconstriction was elicited with histamine (10 microg/kg plus 500 microg/kg/hr iv). Thirty minutes after the start of histamine infusion, 0 (saline), 1, 10, and 100 micromol/kg ZnSO4 or 1, 10, 100, and 1000 micromol/kg MgSO4 or Na2SO4 were administered intravenously in group Zn, Mg, or Na, respectively. The bronchial cross-sectional area was assessed before (basal) and 30 mins after the start of histamine infusion and 5 mins after each dose of ZnSO4, MgSO4, or Na2SO4. Arterial blood was also obtained to measure plasma levels of epinephrine and norepinephrine by gas chromatography-mass spectrometry. All data are expressed as mean +/- SEM. The doses of the divalent cations that reversed histamine-induced contraction by 50% were calculated by GraphPad Prism. MgSO4 and ZnSO4 (9.38+/-0.28 and 1.84+/-0.30 mM, respectively) relaxed histamine-contracted tracheal strip in a concentration-dependent manner, whereas Na2SO4 did not. Similarly, the in vivo study showed that MgSO4 and ZnSO4 dose-dependently reversed histamine-induced bronchoconstriction (potency, ZnSO4 > MgSO4), whereas Na2SO4 did not. In groups Mg and Zn, the plasma catecholamine levels also dose-dependently increased except when 1000 micromol/kg MgSO4 was administered. CONCLUSION: Because the divalent cations tested produced a spasmolytic effect on the contracted airway, infusion of divalent cations might be effective against asthmatic attack. However, high concentrations of these cations produce significant toxicity, so dosage will be an important concern in development of these agents.

Animals↗

PubMed1990

Inhaled sodium metabisulphite induced bronchoconstriction: inhibition by nedocromil sodium and sodium cromoglycate.

1. The effects of nedocromil sodium and sodium cromoglycate on bronchoconstriction induced by inhaled sodium metabisulphite have been studied in eight atopic subjects, three of whom had mild asthma. 2. Nedocromil sodium (4 mg, 7.8 X 10(-6) M), sodium cromoglycate (10 mg, 24.1 X 10(-6) M) and matched placebo were administered by identical metered dose inhalers 30 min before a dose-response to sodium metabisulphite (5-100 mg ml-1) was performed. 3. Maximum fall in sGaw after placebo pre-treatment was -43.9 +/- 3.3% baseline (mean +/- s.e. mean). At the same metabisulphite concentration maximum fall in sGaw after sodium cromoglycate was -13.0 +/- 3.6% and after nedocromil sodium was +4.3 +/- 6.8%. Nedocromil sodium prevented any significant fall in sGaw even after higher concentrations of metabisulphite. 4. Both nedocromil sodium, 4 mg, and sodium cromoglycate, 10 mg, inhibited sodium metabisulphite induced bronchoconstriction but nedocromil sodium was significantly more effective. Relative in vivo potency of the two drugs is broadly in line with other in vivo and in vitro studies.

Administration, Inhalation↗

PubMed1990

Adenosine bronchoconstriction in asthma: investigations into its possible mechanism of action.

1. Inhaled adenosine and its parent nucleotide, adenosine 5'-monophosphate (AMP) provoke bronchoconstriction in atopic and asthmatic individuals but not in normal subjects. 2. In clinical studies, histamine H1-receptor antagonists, cyclo-oxygenase inhibitors and the mast cell 'stabilising' drugs, sodium cromoglycate and nedocromil, protect against the effects of adenosine bronchoprovocation suggesting the involvement of secondary mast cell mediator release. 3. Adenosine and its analogues potentiate histamine and leukotriene release from mast cells activated by other stimuli in vitro, and may also increase net mediator release from mast cells by counteracting the inhibitory effect of circulating adrenaline. 4. Although adenosine fulfils many of the criteria required for a mediator in asthma, its importance is not fully understood, and the mechanisms by which it provokes bronchoconstriction in asthmatic subjects is far from concluded. 5. Two possibilities are that either adenosine acts directly on luminal mast cells to upregulate histamine secretion, or it acts to initiate neuronal reflexes which stimulate histamine release indirectly and possibly activate peptidergic and/or cholinergic pathways.

Adenosine↗

PubMed1992

Inhibition of inhaled metabisulphite-induced bronchoconstriction by inhaled frusemide and ipratropium bromide.

1. The effect of inhaled frusemide and high dose inhaled ipratropium bromide on bronchoconstriction induced by inhaled metabisulphite was studied in 10 atopic volunteers. 2. Frusemide (40 mg), ipratropium bromide (0.5 mg) or saline placebo were administered by nebuliser in a double-blind fashion, prior to construction of a dose-response curve to metabisulphite (2.5-100 mg ml-1). 3. Geometric mean of the provocative dose of metabisulphite that caused a 35% fall in specific airways resistance (sGaw) after placebo was 13 (95% confidence intervals CI 4-36 mumol) compared with 36 (16-78) mumol after ipratropium bromide and 45 (22-94) mumol after frusemide. 4. Mean maximum fall in sGaw was 49 (40-57)% after placebo, 11 (0-22)% after frusemide and -1 (-25-22)% after ipratropium bromide. 5. Frusemide significantly protected against metabisulphite induced bronchoconstriction (P less than 0.005). The protection from high dose ipratropium bromide was also significant (P less than 0.05), but the response was more variable between subjects.

Administration, Inhalation↗

PubMed1994

Effects of a thromboxane receptor antagonist on prostaglandin D2 and histamine induced bronchoconstriction in man.

Many prostanoids including are prostaglandin (PG) F2 alpha and PGD2 are potent bronchoconstrictor agents. There is evidence to suggest that airway thromboxane (TP) receptor may act as a common receptor for their bronchoconstrictor actions. We tested the hypothesis that inhaled prostaglandin (PG) D2-induced bronchoconstriction is mediated by interacting with the TP receptor antagonist, ICI 192605, on the bronchoconstrictor response to inhaled PGD2 in a double-blind, placebo-controlled and crossed-over trial in normal subjects. The effect of ICI 192605 on histamine induced bronchoconstriction served as control for non-specific bronchodilatory actions. The study had two phases; the first consisted of two inhaled PGD2 challenge study days, and the second phase was that of inhaled histamine. Each study day was separated by at least a week. On each study day, the challenge tests were carried out 30 min after ingestion of 100 mg ICI 192605 or placebo. Doubling concentrations of agonist were given till more than 35% fall in post-diluent specific airway conductance (sGaw) occurred. The concentration needed to cause a fall in a sGaw of 35% post-diluent value (PC35sGaw) was then determined from linear interpolation of the log dose-response. Eight male subjects (median age 26, range 20-35 years) completed the study. ICI 192605 did not change baseline airway calibre 30 min after ingestion on either PGD2 or histamine study days. ICI 192605 significantly shifted the dose-response curve to inhaled PGD2 to the right by a median of 3.4 fold (Wilcoxon rank sign test, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Effect of inhaled atrial natriuretic peptide on methacholine induced bronchoconstriction in asthma.

We have previously demonstrated that intravenous and inhaled atrial natriuretic peptide (ANP) significantly inhibits histamine induced bronchoconstriction in asthmatic patients. The current study was designed to determine whether inhaled ANP was also able to inhibit the effects of methacholine. Eight atopic asthmatic patients (five women) were studied: mean (SD) age 38.2 (8.3) years flow expiratory volume per second (FEV1) 2.97 (0.60) litres, equivalent to 92 (13) % of the predicted. Each had demonstrated at least mild bronchial hyperreactivity to inhaled methacholine at screening (geometric mean PC20 1.02 mg/ml; range 0.11-6.54 mg/ml). Patients attended for 3 study days and after baseline spirometry received 3.5 ml saline (placebo), 0.1 mg ANP or 1 mg ANP (ANP dissolved in 3.5 ml saline) in a randomized, double-blind manner via a Mizer aerosol conservation device. Aerosolization took approximately 9 min and FEV1 was repeated at 0.5, 1.5 and 3 min after completion. Immediately thereafter each patient received a 2 min inhalation of methacholine at a dose individually calculated to give a 25% fall in FEV1 (as extrapolated at their initial screening visit) and the FEV1 was followed over the next 20 min. Mean (SEM)% FEV1 did not change significantly after ANP being -4.3 (1.7), -3.2 (2.7) and -2.4 (1.2) after placebo, 0.1 mg ANP and 1 mg ANP respectively. The mean (SEM) maximum fall in FEV1 after methacholine was as follows: placebo 26.9 (5.7)%, 0.1 mg ANP 18.2 (4.3)% and 1.0 mg 11.2 (2.7)% (P < 0.05 placebo vs 1 mg ANP). These results demonstrate that ANP offers significant protection against methacholine induced bronchoconstriction in asthmatic patients.

Administration, Inhalation↗

PubMed1991

Reproducibility of leukotriene D4 inhalation challenge in asthmatics. Effect of a novel leukotriene D4/E4-antagonist (SR 2640) on leukotriene D4-induced bronchoconstriction.

We have studied the reproducibility of a bronchial leukotriene (LT) provocation test in asthmatics, and the effect of prior treatment with an oral leukotriene D4/E4 antagonist (SR 2640) on LTD4-induced bronchoconstriction in nine asthmatics in a double-blind placebo-controlled randomized cross-over trial. The reproducibility of the bronchial leukotriene provocation test was high. For a specific patient, the replication variance is 0.2303, and the standard deviation is thus 0.4799, corresponding to 48%, i.e. one halving of the dose or half doubling of the dose. SR 2640 antagonised LTD4 induced bronchoconstriction causing a mean shift of 48% to the right of the dose-response curve as compared with placebo (95% confidence interval being 11-137%). This study demonstrates that bronchial LTD4 provocation test is a safe and reproducible method in asthmatics, and that the method can be used to detect LT-antagonism; furthermore that SR 2640 is a weak LTD4-antagonist in asthmatics.

Adult↗

PubMed2005

Asthma in medium altitude--exercise-induced bronchoconstriction in hypobaric environment in subjects with asthma.

BACKGROUND: Hypoxic gas inhalation has been reported to enhance airway responsiveness and results in bronchoconstriction in animal models and in humans with asthma. However, the data have so far been conflicting. The aim of the present study was to examine the effect of reduced barometric pressure on exercise-induced bronchoconstriction (EIB) in subjects with asthma. METHODS: Twenty subjects (10-45 years old, male symbol/female symbol = 13/7) with asthma (at least 10% reduction in forced expiratory volume in 1-second postexercise) participated in exercise testing in barometric pressure corresponding to altitudes of 200 (normobaric) and 2500 (hypobaric) m above sea level in random order on separate days. Lung function was measured before and after exercise, as well as after inhalation of salbutamol. Heart rate, oxygen uptake (), arterial oxygen saturation (S(p)O(2)), respiratory gas exchange ratio (RER) and minute ventilation () were measured during exercise. RESULTS: There was no difference in lung function after exercise. The and HR(peak) during exercise did not differ. The RER(peak) was higher (P = 0.04) in hypobaric environment. The decreased 10.1% (7.2-13.0) [mean (95% confidence intervals)] (P < 0.001) from normobaric to hypobaric environment. At the same time, S(p)O(2) at decreased from 94.4 (92.2-96.6) to 85.6% (82.8-88.4) (P < 0.001). CONCLUSIONS: A barometric pressure corresponding to altitude of 2500 m did not increase EIB in subjects with asthma. The reduction in is most probably due to the lower S(p)O(2) in hypobaric environment.

Adolescent↗

PubMed1991

Toxic oxygen metabolites induce vasoconstriction and bronchoconstriction in isolated, plasma-perfused rat lungs.

Effects of toxic oxygen metabolites (TOM) on the pulmonary vascular bed and airways were studied in isolated, plasma-perfused rat lungs. TOM were generated by xanthine oxidase (XO) (0.1 or 0.25 unit.ml-1) and hypoxanthine (HX) (1 mol.l-1). In vitro measurements by chemiluminescence indicated that the major oxygen metabolite generated by XO and HX was H2O2. Measurements of PO2 in the perfusate as an indicator of O2-consumption suggested that production of TOM by XO and HX was finished within 30 min. XO and HX induced an early dose-dependent bronchoconstriction and a late increase in transpulmonary pressure (Ptp). Pulmonary arterial pressure (Ppa) increased gradually and levelled off within 30 min with low-dose XO, but not with high-dose XO. As judged by weight increase of the lungs, interstitial edema occurred regularly. Allopurinol, an inhibitor of XO, blocked the lung responses caused by XO and HX. Catalase attenuated all lung responses induced by XO and HX, while superoxide dismutase had no effect. The hydroxyl radical scavenger dimethylsulfoxide abolished the increase in Ptp and attenuated the increase in Ppa, but did not consistently protect the lungs from edema development. This study shows that TOM induce vasoconstriction, bronchoconstriction and lung edema in plasma-perfused rat lungs, mainly due to generation of H2O2 and the hydroxyl radical.

Animals↗

PubMed2006

Protective effects of volatile agents against acetylcholine-induced bronchoconstriction in isolated perfused rat lungs.

BACKGROUND: Bronchoactive properties of volatile agents against lung constriction are well established. The purpose of this study was to investigate the ability of halothane (Hal), isoflurane (Iso), sevoflurane (Sev) and desflurane (Des) to alter the lung mechanics in the absence of an airway tone and during acetylcholine (Ach)-induced bronchoconstriction. METHODS: Low-frequency pulmonary impedance data (ZL) were collected from isolated, normo-perfused rat lungs under baseline conditions and following the injection of Ach (0.1 mg/kg) into the pulmonary artery. Measurements were performed without the administration of any anaesthetic agent in the first phase of the experiments and during inhalation without any volatile agent (control group, n = 6) or during inhalation of Hal (n = 6), Iso (n = 9), Sev (n = 6) or Des (n = 8) at 1 minimum alveolar concentration (MAC). The airway resistance (Raw) and parenchymal damping and elastance were estimated from the Z(L) data by model fitting. RESULTS: Under baseline conditions, the basic value of Raw was significantly decreased by Des (- 31.2 +/- 3.8%) and Sev (- 18.0 +/- 4.5%) administration, whereas Hal and Iso did not have a statistically significant effect on Raw (- 3.3 +/- 5.1% and - 8.6 +/- 2.4%, respectively). Moreover, all four inhalation anaesthetics prevented the increase in Raw following Ach administration, the findings ranging between - 14.3 +/- 11.4% for Hal and - 37.5 +/- 10.9% for Sev. CONCLUSIONS: Our results on a denervated isolated perfused lung model demonstrate the potential of Des and Sev to decrease the basal airway tone, whereas Iso and Hal are ineffective in this regard. All of these volatile agents markedly protect against Ach-induced bronchoconstriction.

Acetylcholine↗

PubMed1990

The effect of inhaled fenoterol and ipratropium bromide on propranolol induced bronchoconstriction in the asthmatic airways.

1. The provocative dose of inhaled propranolol, (PC20P, mg/mL) needed to induce a 20% reduction in the forced expired volume in 1 s (FEV1, L) was determined for 15 adult asthmatics following randomized pre-treatment with placebo, ipratropium bromide (40, 160 micrograms) and fenoterol (200, 800 micrograms) aerosols using a double-blind protocol. 2. Fenoterol 200 micrograms, 800 micrograms increased the baseline FEV1 0.28 +/- 0.16, 0.32 +/- 0.16 L (P = 0.04, P = 0.008 respectively). Fenoterol 800 micrograms moved the PC20 P rightwards from placebo geometric mean 10.95, 95% Confidence Intervals (95% CI) 4.43-27.22 mg/mL to mean 20.41, 95% CI 10.13 to 40.64 mg/mL (P = 0.01). Fenoterol 200 micrograms was not protective; mean PC20 16.22, 95% CI 7.83-34.35 mg/mL (P = 0.08). Neither 40 or 160 micrograms ipratropium changed the FEV1 or PC20P values compared with placebo; increase in FEV1 0.15 +/- 0.27 L (P = 0.22), 0.24 +/- 0.12 L (P = 0.14) and geometric mean PC20P 16.59 +/- 0.57 mg/mL, 95% CI 8.01-34.51 mg/mL (P = 0.90), 15.58 +/- 0.66 mg/mL, 95% CI 6.72-36.05 mg/mL (P = 0.34) respectively after ipratropium treatments. 3. Bronchoconstriction induced by inhaled propranolol (P) appears to be only weakly antagonized by inhaled beta-agonist and not reduced by antimuscarinic anticholinergic aerosol. This finding argues against the activation of a cholinergic reflex to explain propranolol induced bronchoconstriction (PIB).

Administration, Inhalation↗

PubMed1996

Tachykinin receptors and non-cholinergic bronchoconstriction in the anaesthetized guinea-pig.

1. Bronchoconstriction can be evoked by electrical stimulation of the vagus nerves in the presence of atropine. We have used novel, highly selective tachykinin receptor antagonists, together with a procedure for on-line, breath-by-breath analysis of total lung resistance (R(L), subtractor method) and dynamic lung compliance (C(dyn)), to investigate the role of tachykinins in this response in anaesthetized, paralysed guinea-pigs. 2. In the presence of 1 mg/kg phosphoramidon (a neutral endopeptidase inhibitor), CP 96345 (the non-peptide NK1 selective antagonist) at 200 nmol/kg had no effect on the increase in R(L) caused by vagal stimulation, but significantly inhibited the associated decrease in C(dyn). 3. The NK2 selective antagonist, MDL 29913 (1 mu mol/kg), significantly antagonized the changes in both R(L) and C(dyn). In the absence of phosphoramidon, MDL 29913 again significantly inhibited the changes in R(L) and C(dyn) although CP 96345 no longer had any effect. 4. The non-peptide NK2 selective antagonist, SR 48968 (100 nmol/kg), also effectively inhibited the responses to vagal stimulation and was more potent than MDL 29913. 5. These results emphasize the importance of the NK2 receptor system in mediating non-cholinergic bronchoconstriction evoked by vagal stimulation in the guinea-pig.

Animals↗

PubMedDate not supplied

Calcitonin gene-related peptide antagonizes the protective effect of adrenomedullin on histamine-induced bronchoconstriction.

1. In the present study the possible relationship between adrenomedullin (AM) and calcitonin gene-related peptide (CGRP) in the regulation of airway functions in anaesthetized guinea-pigs was examined in vivo. 2. We found that AM significantly inhibited histamine-induced bronchoconstriction in a dose-dependent manner. CGRP or the CGRP receptor antagonist (CGRP [8-37]) alone did not affect pulmonary resistance and pretreatment with CGRP or CGRP [8-37] did not significantly affect histamine-induced bronchoconstriction. However, AM-induced bronchoprotection was significantly inhibited by pretreatment with CGRP or CGRP [8-37] in a dose-dependent manner. 3. It is therefore possible that CGRP may be competitive, at least in part, with binding sites of AM in the guinea-pig airway. Exogenous AM may be useful for the management of bronchial asthma, not only as a potent bronchodilator, but also as a functional antagonist of CGRP.

Adrenomedullin↗

PubMed2004

Preventive effect of lacrimal occlusion on topical timolol-induced bronchoconstriction in asthmatics.

AIM: To evaluate the potential preventive role of lacrimal occlusion on the topical timolol-induced bronchoconstriction in asthmatics. METHODS: This was a prospective and single-masked study. Fourteen volunteer subjects with asthma were included. Collagen plugs were inserted into both canaliculi on one side to inhibit lacrimal drainage. The effect of lacrimal occlusion on lung function tests was measured before and 60 min after the instillation of a timolol drop in unplugged and plugged eyes. The spirometric measurements include forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), FEV1/FVC, and mid expiratory flow-rate (FEF25-75). RESULTS: The timolol (0.5%) drop administration into the eye caused a significant decrease in pulmonary functions in patients with asthma in whom the lacrimal punctae had not been occluded by collagen plug. P values were 0.008 for FVC and 0.001 for FEV1 and FEF25-75. The occlusion of the lacrimal duct by intracanalicular plugs significantly reduced this decrease in pulmonary function. P values were 0.6 for FVC, 0.8 for FEV1, and 0.5 for FEF25-75. The lacrimal occlusion did not affect heart rate and blood pressures. Three subjects complained of epiphora. CONCLUSIONS: Lacrimal occlusion with intracanalicular collagen plugs may almost completely prevent the bronchoconstriction caused by topical timolol in asthmatics by inhibiting or decreasing systemic absorption of the medication.

Administration, Topical↗

PubMed1998

Effects of carbamazepine on plasma extravasation and bronchoconstriction induced by substance P, capsaicin, acetaldehyde and histamine in guinea-pig lower airways.

We evaluated the in vivo effects of the pretreatment with carbamazepine (CBZ) at different doses (10, 20 and 40 mg/kg p.o.) on the Evans-blue extravasation and on bronchoconstriction induced by different substances in guinea-pig tracheal tissue. The drug dose-dependently inhibited the extravasation induced by substance P (SP), capsaicin and acetaldehyde, but not that induced by histamine. At the highest dose (40 mg/kg) CBZ inhibited the bronchoconstriction induced by SP, capsaicin and acetaldehyde, but not that produced by histamine administration. The in vitro study with guinea-pig tracheal preparation indicates that the drug does not interfere with the binding of SP to its receptors. Our results suggest that CBZ exerts a protective activity against the pro-inflammatory action of SP.

Acetaldehyde↗