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PubMed1977

The effects of sodium cromoglycate on histamine aerosol-induced reflex bronchoconstriction in the anaesthetized dog.

1 The effects have been studied of sodium cromoglycate (SCG), given by aerosol or intravenously, on reflex bronchoconstriction induced by histamine aerosol in the anaesthetized dog. 2 Four breaths of an aerosol generated from a 2% solution of SCG significantly inhibited the vagally mediated increase in total lung resistance (RL) produced by histamine. 3 SCG given intravenously as bolus injections (5-500 microgram/kg) produced a dose-dependent reversal of a sustained reflex bronchoconstriction induced by histamine aerosol. Propranolol (500 microgram/kg) did not prevent this reversal. 4 SCG did not inhibit the increase in RL produced by supramaximal electrical stimulation of a vagus nerve. 5 The possibility is discussed that SCG may reduce the activity of lung irritant receptors in the anaesthetized dog.

Aerosols↗
PubMed1980

A model of irritant-induced bronchoconstriction in the spontaneously breathing guinea-pig.

1 Inhalation of an aqueous aerosol of citric acid caused bronchoconstriction in anaesthetized guinea-pigs which was abolished by bilateral vagal section. 2 Conscious guinea-pigs developed slow, laboured breathing within 90 s of exposure to citric acid aerosol. The onset of this pattern of breathing was delayed by prior aerosol administration of atropine, ipratropium bromide, isoprenaline and tetracaine. 3 The data suggest that exposure of guinea-pigs to citric acid may be a useful model of reflex bronchoconstriction.

Animals↗
PubMed1983

Sodium cromoglycate, verapamil and nicardipine antagonism to leukotriene D4 bronchoconstriction.

1--The effects of nicardipine, verapamil and sodium cromoglycate (SCG) on the increase in pulmonary airway resistance(RAw) and decrease in pulmonary dynamic compliance (CDyn) induced by leukotriene D4 (LTD4) 0.5 micrograms kg-1 and acetylcholine (ACh) 3 micrograms kg-1 were investigated in anaesthetized guinea-pigs. The effects of these three agents on the contractile effects of LTD4 and ACh were tested on isolated tracheal preparations of the guinea-pig. 2--Nicardipine and verapamil (0.3 and 1 mg kg-1), as well as SCG (3 and 10 mg kg-1), partially but significantly inhibited the effects of LTD4 on RAw. Partial inhibition of the effect of LTD4 on CDyn was only observed with verapamil (0.3 and 1 mg kg-1). Nicardipine and verapamil had no effect on ACh-induced bronchoconstriction in vivo. 3--In concentrations higher than 10(-5) M, nicardipine and verapamil inhibited the contractile effects of LTD4 and ACh on guinea-pig isolated trachea. SCG had no effect on this preparation. 4--These results suggest that nicardipine, verapamil and SCG partially reduce the component of bronchoconstriction associated with stimulation of irritant receptors by LTD4. However, the site and mechanism of action of Ca2+-entry antagonists remain uncertain.

Airway Resistance↗
PubMed1987

Airways hyperreactivity and bronchoconstriction induced by vanadate in the guinea-pig.

1 The characteristics of vanadate-induced bronchoconstriction and airways hyperreactivity were observed in spontaneously breathing anaesthetized guinea-pigs by measurement of airways resistance (Raw) and dynamic lung compliance (Cdyn). Vanadate (0.3-3 mg kg-1 i.v. over 25 min) increased Raw and decreased Cdyn in a reversible, dose-related manner. This action (1 mg kg-1 vanadate) was not inhibited by atropine (1 mg kg-1 i.v.), propranolol (1 mg kg-1 i.v.) or bilateral vagotomy, suggesting a direct effect on the airways smooth muscle. 2 An aerosol of vanadate (10% w/v in H2O) for 3 min decreased Cdyn by 19.5% (P less than 0.05, n = 6) but caused no change in Raw. 3 Histamine (3 micrograms kg-1 i.v.) caused a bronchoconstriction which was enhanced by vanadate in a dose-related manner. This hyperreactivity (after 1 mg kg-1 i.v. vanadate) was unchanged after propranolol or bilateral vagotomy, but was partly blocked by atropine (enhancement by vanadate of the Cdyn change to histamine was diminished, P less than 0.02, n = 3). 4 Bronchoconstrictor responses to acetylcholine (6 micrograms kg-1 i.v.) and 5-hydroxytryptamine (6 micrograms kg-1 i.v.) were also enhanced by vanadate (1 mg kg-1 i.v.) Hyperreactivity after vanadate to the three bronchoconstrictors tested continued during vanadate infusion and was reversed 45 min after cessation of infusion. 5 Histamine (3 ;Lgkg-' i.v.) caused a transient tachypnoea which was also enhanced by vanadate (0.3-3mgkg-'i.v.), in a dose-related manner, in association with the increased reactivity of the airways (r = 0.66, n = 11). 6 It is concluded that vanadate-induced airways hyperreactivity is non-vagal (efferent) and largely non-cholinergic in origin and appears to involve an action of vanadate within the lung itself.

Acetylcholine↗
PubMed1982

Actions of theophylline, terbutaline, and ipratropium bromide alone and in combinations on the methacholine induced bronchoconstriction in rats.

Rats under pentobarbitone anaesthesia, pancuronium relaxation and artificial ventilation with constant volume, were given methacholine (MeCh) 4, 6, and 9 micrograms intravenously at 2 min. intervals; the rise in intratracheal pressure indicated bronchoconstriction. The heights of peak responses (PIPR), response areas (RA), and blood pressure and heart rate were recorded, and theophylline (THEO) concentrations in plasma and lung tissue were measured. THEO (5, 10, or 20 mg/kg intravenously) proved a weak bronchodilator agent with pronounced effects on circulation. Terbutaline (TER) (10, 20, or 40 microgram/kg intravenously) shifted dose dependently the airways MeCh dose-response curves to the right, with minor stimulation of the heart. THEO 5+TER 20, and THEO 20+TER 20 enhanced the bronchodilator action of each other in an additive manner. Ipratropium bromide (IPRA) (5 micrograms/kg intravenously) eliminated MeCh bronchoconstriction without any inhibition of MeCh bradycardia and with partial inhibition of MeCh hypotonia. THEO 20+IPRA 0.5 provided a supra-additive bronchodilation. Injection of TER 20 promoted the penetration of THEO into the lungs thus increasing THEO concentrations in the lung tissue. The present results suggest that in this animal model combinations of low doses of THEO with TER/IPRA provide enhanced bronchodilation but reduced cardiovascular effects, in comparison with single therapy. Further, a pharmacokinetic interaction between THEO and a beta 2-agonist was evident within certain doses.

Animals↗
PubMed1976

Vagal reflexes in the bronchoconstriction occurring after induced intravascular platelet aggregation.

Intravascular platelet aggregation induced in cats by i.v. infusions of collagen caused a transient increase in pulmonary vascular resistance (PVR) and in non-elastic pulmonary resistance (RL), and a transient decrease in dynamic lung compliance (dyn CL). PVR,dyn CL and platelet aggregation after collagen infusions were unaffected by bilateral cervical vagotomy and atropinization, wheras these procedures reduced the post-infusion rise in RL by about 50 per cent. The administration of indomethacin inhibited platelet aggregation as well as bronchoconstriction after collagen infusion. The present investigation indicates that intravascular platelet aggregation will cause reflex bronchoconstriction mediated by vagal efferent fibres.

Animals↗
PubMed1969

Activity of lung irritant receptors in pulmonary microembolism, anaphylaxis and drug-induced bronchoconstrictions.

1. Lung irritant receptors have been studied in rabbits by recording action potentials from single vagal nerve fibres. Some of the rabbits were bilaterally vagotomized, and some paralysed and artificially ventilated.2. The receptors gave rapidly adapting irregular discharges on inflation and deflation of the lungs. Many were stimulated by insufflation of ammonia vapour into the lungs, and some by passage of a fine catheter into the right bronchial tree. The fibres had conduction velocities in the range 3.6-25.8 m/sec.3. The receptors were strongly stimulated by intravenous injections of histamine acid phosphate, 25-100 mug/kg. The response was considerably reduced by previous injection of isoprenaline which also reduced the bronchoconstriction due to histamine.4. The receptors were stimulated by intravenous injections of isoprenaline, phenyl diguanide and micro-emboli, and by anaphylaxis induced in rabbits previously sensitized to egg albumin.5. The receptor responses could not be closely correlated in size with simultaneous changes in total lung resistance, lung compliance, tidal volume or breathing frequency.6. It is concluded that, in rabbits with intact vagus nerves, lung irritant receptors contribute to the reflex hyperpnoea and bronchoconstriction of the conditions studied.

Action Potentials↗
PubMed1992

Inhaled frusemide against cold air induced bronchoconstriction in asthmatic children.

Inhaled frusemide prevents bronchoconstriction in asthmatic adults induced by various triggers. To determine if frusemide provides similar protection in children, whether this is age dependent and equally effective for central and peripheral airways, we performed a double blind, placebo controlled, randomised, crossover study on the effect of inhaled frusemide on lung function changes induced by cold air challenge in 21 asthmatic children. In addition, we measured diuresis before and after inhalation. Bronchodilatation after frusemide was not observed. However, deterioration in lung function after frusemide, compared with placebo, was significantly diminished: forced expiratory volume in one second (FEV1) was -5.7% v -11.5%, peak expiratory flow (PEF) -7.7% v -23.3%, maximum expiratory flow at 50% of vital capacity (MEF50VC) -16.0% v -35.2%, and at 60% of total lung capacity (MEF60TLC) -32.4% v -61.6%, and specific airways conduction -42.0% v -57.7%, respectively. This effect was not age dependent. Diuresis was significantly increased from a mean (SEM) of 198 (34) ml/3 hours before inhaled frusemide to 379 (62) ml/3 hours after nebulisation. We conclude that inhaled frusemide prevents cold air induced bronchoconstriction in asthmatic children and that increased diuresis can be expected with a dose as low as 28 mg of frusemide given by nebuliser.

Adolescent↗
PubMed1979

Bronchoconstriction in potroom workers.

The effect on airway responsiveness of an oral dose of a beta-adrenergic blocker (80 mg propranolol) given before work, was studied in 15 potroom workers who complained of dyspnoea, chest tightness and wheezing after they had started to work in potrooms. The same study was performed in a group of 10 potroom workers, selected at random, who had not complained of such symptoms. In addition, another group of 12 potroom workers with respiratory symptoms were given 1 mg atropine subcutaneously. Ventilatory function was assessed from forced expiratory curves (by means of a waterless spirometer) and from maximum expiratory flow-volume curves (by means of a digital pneumotachograph). Bronchoconstriction during the first few hours' work was significantly potentiated by propranolol in the group of potroom workers with respiratory complaints. Propranolol did not produce this effect in workers who had not complained of respiratory symptoms. Atropine sulphate abolished the fall in ventilatory volumes which occurred during the first few hours of work. These findings suggest that acute bronchoconstriction, particularly in small airways, and respiratory symptoms occurring in certain potroom workers may be based on an alteration in autonomic balance with vagal preponderance.

Adult↗
PubMed1977

Inhibition of aspirin-induced bronchoconstriction by sodium cromoglycate inhalation.

Five patients with asthma and severe aspirin hypersensitivity were challenged on separate days with increasing doses of aspirin given by mouth, starting with 5 mg, until a reduction in FEV1 greater than 15% was obtained. Sodium cromoglycate in doses of 20-40 mg inhibited the bronchoconstrictive reaction not only when inhaled before the challenge but also after it, at a time when progressive reduction in FEV1 values was taking place. According to these results, it seems reasonable to postulate sequential mast cell degranulation and liberation of mediators of anaphylaxis as the mechanism through which aspirin induces bronchoconstriction in aspirin-sensitive asthmatics. The differences between bronchial provocation tests and oral challenge with aspirin are stressed.

Adolescent↗
PubMed1981

Exercise-induced bronchoconstriction as an expression of bronchial hyperreactivity: a study of its mechanisms in children.

The mechanism of exercise-induced bronchoconstriction (EIB) was studied by observing the protective effects of several aerosol agents in a double-blind, randomised trial. Exercise-induced bronchoconstriction was not affected by placebo, but was reduced by each agent used (p less than 0.001). Blocking the parasympathetic system had the weakest effect, while beta 2 adrenergic stimulation produced the strongest effect which was significantly different from the parasympatholytic (p less than 0.02). The effect of the mast cell stabilizer, sodium cromoglycate (SCG) was found to be intermediate. However in some patients SCG had a stronger effect than the beta 2 adrenergic agonist. A relationship was found between EIB and bronchial hyperreactivity induced by histamine (p less than 0.05).

Adolescent↗
PubMed1982

Factors influencing the bronchodilator effect of a deep inspiration in asthmatic patients with provoked bronchoconstriction.

We have studied 26 asthmatic patients in whom deep inspiration induced a transient but marked bronchodilatation when carbachol-induced bronchoconstriction was present. Changes in bronchial tone were assessed by specific airway resistance measurements. Bronchodilatation after a slow inspiration (eight subjects) or a 10-second breath-hold at total lung capacity (13 subjects) was significantly less than that observed after either a fast inspiration or no breath-holding period. The magnitude of the bronchodilatation induced by a fast inspiration without breath-holding was directly and significantly related to the magnitude of the carbachol-induced bronchoconstriction in five subjects.

Adult↗
PubMed1984

Effect of prior bronchoconstriction on the airway response to histamine in normal subjects.

We have examined the effect of prior bronchoconstriction on the bronchial responsiveness to inhaled histamine in nine normal subjects. The airway response to increasing concentrations of histamine aerosol was assessed by measurement of specific airways conductance (sGaw) in a body plethysmograph. The threshold provocative dose of histamine needed to cause a 35% fall in starting sGaw (PD35) and the steepest slope of the response were measured from cumulative log dose response curves. Histamine challenges were performed in duplicate after premedication with 0.9% sodium chloride (control) or methacholine aerosol on separate days. The mean starting sGaw did not change significantly after inhalation of 0.9% sodium chloride but methacholine caused a mean reduction in sGaw of 42%. Mean control PD35 values did not differ significantly from mean PD35 values after methacholine. The mean steepest slope of the response after methacoline was 47% lower than the mean control value. There was a significant linear relationship between starting sGaw and the steepest slope for the control and for the methacholine premedicated challenges. The reduction in slope after methacholine was accounted for by the fall in starting sGaw. Because histamine PD35 was not altered by prior bronchoconstriction, it is concluded that the bronchial hyperresponsiveness of asthmatic subjects to non-specific bronchoconstrictor stimuli is unlikely to be a direct consequence of their low starting airway calibre.

Adult↗
PubMed1986

Effect of inhaled piriprost (U-60, 257) a novel leukotriene inhibitor, on allergen and exercise induced bronchoconstriction in asthma.

The leukotrienes, a group of oxidative metabolites of arachidonic acid, have potent pharmacological actions on human airways. We have investigated the effects of a leukotriene synthesis inhibitor, piriprost (U-60, 257) administered by inhalation on allergen and exercise induced bronchoconstriction in 12 subjects with allergic asthma. Subjects underwent diagnostic challenges with allergen and treadmill exercise to define the strengths of the stimuli required to reduce the FEV1 to about 25% of baseline (PS25). On separate study days subjects inhaled either piriprost 1 mg or vehicle placebo, followed 15 minutes later by the PS25 allergen or exercise. The FEV1 was measured at regular intervals before and after challenge up to 60 minutes. After allergen challenge in six subjects peak expiratory flow (PEF) was measured for the following 20 hours. When compared with placebo, inhalation of piriprost had no significant protective effect on the fall in FEV1 at any time point within 60 minutes of allergen or exercise challenge. In the four subjects with a documented late asthmatic reaction 2-12 hours after allergen challenge piriprost had no protective effect when compared with placebo. In the subjects who recorded PEF over 20 hours after allergen challenge there was no significant difference between piriprost and placebo. Piriprost was appreciably more irritant to the respiratory tract than was placebo. On the assumption that inhaled piriprost was bioavailable in the airways, this study casts doubt on any theory of a pivotal role for leukotrienes in the pathogenesis of acute exercise and allergen induced airway bronchoconstriction in asthma.

Administration, Inhalation↗
PubMed1986

Effect of sleep deprivation on overnight bronchoconstriction in nocturnal asthma.

Nocturnal cough and wheeze are common in asthma. The cause of nocturnal asthma is unknown and there is conflicting evidence on whether sleep is a factor. Twelve adult asthmatic subjects with nocturnal wheeze were studied on two occasions: on one night subjects were allowed to sleep and on the other they were kept awake all night, wakefulness being confirmed by electroencephalogram. Every patient developed bronchoconstriction overnight both on the asleep night, when peak expiratory flow (PEF) fell from a mean (SE) of 418 (40) 1 min-1 at 10 pm to 270 (46) 1 min-1 in the morning, and on the awake night (PEF 10 pm 465 (43), morning 371 (43) 1 min-1). The morning values of PEF were, however, higher (p less than 0.1) after the awake night and both the absolute and the percentage overnight falls in PEF were greater when the patients slept (asleep night 38% (6%), awake night 20% (4%); p less than 0.01). This study suggests that sleep is an important factor in determining overnight bronchoconstriction in patients with nocturnal asthma.

Adult↗
PubMed1987

Effectiveness of a heat and moisture exchanger in preventing hyperpnoea induced bronchoconstriction in subjects with asthma.

The effect of a heat and moisture exchanger, a device with hygroscopic material for conditioning inspired air, on hyperpnoea induced bronchoconstriction was studied in nine non-smoking volunteers with asthma, aged 19-32 years. Each had previously shown an increase of at least 100% in specific airways resistance (sRaw) to isocapnic hyperpnoea with dry air. On two separate days the subject performed isocapnic hyperpnoea with dry air at 60-70 l min-1 for five minutes. Before, immediately after, and five minutes after completion of a test sRaw measurements were made. Heat and moisture exchangers were placed in the breathing circuit on one of the two days. All subjects had an increase in sRaw of 100% or more without the heat and moisture exchangers (average increase 300%) but were protected from bronchoconstriction with the devices in place (average increase 7%) (p less than 0.005). The exchanger's resistance to airflow was less than 1 cm H2O for flow rates of 100 l min-1. A heat and moisture exchanger designed as a facemask or mouthpiece may allow a person with asthma to exercise without the need for prophylactic drugs.

Adult↗
PubMed1987

Effects of a cyclo-oxygenase inhibitor, flurbiprofen, and an H1 histamine receptor antagonist, terfenadine, alone and in combination on allergen induced immediate bronchoconstriction in man.

The effect of flurbiprofen, a potent cyclo-oxygenase inhibitor, on histamine and methacholine reactivity was assessed in seven atopic subjects with asthma. Flurbiprofen 150 mg daily for three days displaced the histamine-FEV1 concentration-response curve to the right by 1.5 doubling doses, whereas no effect was observed on the response to methacholine. Subsequently the effects of flurbiprofen and terfenadine, a specific H1 histamine receptor antagonist, on allergen induced bronchoconstriction were studied in seven atopic but non-asthmatic subjects. The subjects inhaled the concentration of grass pollen allergen that had previously been shown to produce a 20% fall in FEV1 on separate occasions after prior treatment with placebo, flurbiprofen 150 mg daily for three days, terfenadine 180 mg three hours before challenge, and the combination of flurbiprofen and terfenadine. After placebo, allergen challenge caused a mean (SEM) maximum fall in FEV1 of 37.6% (2.6%) after 20 (3.7) minutes, followed by a gradual recovery to within 15% of baseline at 60 minutes. Terfenadine reduced the maximum allergen provoked fall in FEV1 to 21.5% (2.2%) and reduced the area under the time-response curve (AUC) by 50% (6%). Flurbiprofen alone reduced the mean maximum fall in FEV1 to 29.6% (3.2%) and reduced the AUC by 26%. The effect of the combination of flurbiprofen and terfenadine did not differ significantly from that of terfenadine alone. We conclude that histamine and prostaglandins contribute to immediate allergen induced bronchoconstriction and that a complex interaction occurs between the two classes of mediators.

Adult↗
PubMed1987

Effect of nedocromil sodium on sulphur dioxide induced bronchoconstriction.

Nedocromil sodium is a pyranoquinoline derivative that has been developed for the treatment of asthma. We report the results of a double blind randomised study of the effect of two doses of nedocromil sodium (2 and 4 mg) and matched placebo, delivered by metered dose pressurised aerosol, on bronchoconstriction induced by sulphur dioxide in six asthmatic subjects. Nedocromil sodium had no effect on baseline lung function. The magnitude of sulphur dioxide induced bronchoconstriction monitored by partial forced expiratory flow at 30% of reference vital capacity was significantly inhibited by nedocromil sodium 4 mg (p less than 0.05) but not by 2 mg. The maximum changes after placebo and after nedocromil 2 mg and 4 mg were -44.7, -32.7, and -11.8 l min-1. The area under the curve monitoring the effect over 6 minutes was significantly inhibited by both doses to the same extent, the mean changes after placebo and after nedocromil 2 mg and 4 mg being -349.3, -31.2, and 44.6 l. Dyspnoea was monitored by visual analogue scale and showed a significant reduction over 6 minutes with both doses of nedocromil. After placebo and after nedocromil 2 mg and 4 mg the mean maximum changes were 31.5, 13.7, and 15.7 mm, and the mean changes in area under the visual analogue scale-time curve were 289, 194, and 151 mm.min respectively.

Adult↗