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PubMed1975

Bronchoconstriction induced by repeated forced vital capacity manoeuvres.

An asthmatic atopic patient who developed bronchoconstriction during repeated forced vital capacity manoeuvres and after exercise is reported. Since increases in total airway and upper segment resistances and drop in FEV1 and Vmax 50 were induced, it is considered that bronchoconstriction involved most of the airways. Partial prevention of this effect could be demonstrated after inhalation of an adrenergic bronchidilator or disodium cromoglycate. Atropine completely prevented the flow response but did not alter the total airway resistance increase. Bronchoconstriction is interpreted as partially related to mast cell disruption and cholinergically mediated stimuli.

Adolescent↗

PubMed1981

Influence of relative humidity and repeated exercise on exercise-induced bronchoconstriction.

The relationship between previous exercise-induced bronchoconstriction (EIB) of different magnitude and the pulmonary response to exercise 1 h later was examined in asthmatic children. After acclimatization they performed repeated, paired exercise tests in a clean-air climatic chamber at 23 degree C. The first test of each pair was carried out in 15%, 50% and 85% relative humidity (RH), respectively, to produce different degrees of EIB. All second tests were performed in 50% RH. Changes in pulmonary function were assessed by measuring PEF and FEV1. Bronchodilatation during exercise was not influenced by RH, whereas dry air increased and humid air decreased the bronchoconstrictive response to exercise. When both tests were performed in 50% RH, the second test caused significantly less EIB than did the first test. However, no differences were found between the three second test responses. This suggests that the relative refractoriness after an episode of EIB is not related to the severity of previous bronchoconstriction, but could be associated with exercise as such or other mechanisms in EIB.

Adolescent↗

PubMed1968

Antagonism by fenamates and like-acting drugs of bronchoconstriction induced by bradykinin or antigen in the guinea-pig.

1. Nine non-steroidal anti-inflammatory drugs were tested for antagonism of bradykinin-induced bronchoconstriction in guinea-pig lungs in vivo. Only one, benzydamine, was inactive.2. The descending order of potency of the active anti-inflammatory drugs was meclofenamate = Scha 306>Scha 87/2>indoxole>Mi85>indomethacin>glafenine>ibufenac.3. Of eight other drugs tested, chlorpromazine, phenoxybenzamine and four others were inactive, whereas phenelzine and mebanazine possessed activity.4. In tests at two dose-levels of meclofenamate, the dose-ratio of bradykinin increased proportionately with the dose of meclofenamate.5. The anti-bradykinin effect of meclofenamate was still observed after destruction of the brain and spinal cord, after bilateral adrenalectomy or after blockade of beta-receptors for adrenaline.6. Meclofenamate did not release catecholamines from the adrenal medulla or prevent such a release by bradykinin given intra-arterially.7. The fenamates and like-acting drugs reduced the intensity of anaphylactic bronchoconstriction in guinea-pigs treated with mepyramine or propranolol. The descending order of potency was meclofenamate>flufenamate>mefenamate.8. Dose / response curves for the antagonism of anaphylactic bronchoconstriction by the fenamates, in the presence of propranolol, turned downwards at high doses.9. These findings suggest that the fenamates may find a useful place in the treatment of bronchial asthma or other conditions involving allergic ventilatory impairment.

Adrenal Medulla↗

PubMed1972

The inhibition by dexamethasone and disodium cromoglycate of anaphylactic bronchoconstriction in the rat.

1. A method for the measurement of anaphylactic bronchoconstriction in the rat is described.2. Dexamethasone inhibited this response in a dose-related manner.3. Disodium cromoglycate antagonized the response. A bell-shaped dose-response curve was obtained with peak activity at 1 mg/kg i.v.4. Meclofenamate was not active when given alone or in combination with dexamethasone.5. Methysergide significantly inhibited the response. Mepyramine, atropine, propranolol and adrenalectomy did not significantly modify the response.6. The relationships of anaphylactic bronchoconstriction in the rat to anaphylactic bronchoconstriction in the guinea-pig and to human asthma are discussed.

Adrenalectomy↗

PubMed1984

Modification by betamethasone of the effects of bronchodilator drugs on cholinergic bronchoconstriction in rats.

Effects of betamethasone (BM), a long-acting glucocorticoid, given alone and in combination with bronchodilator drugs, terbutaline (Ter), theophylline (Theo), or ipratropium bromide (Ipra), were studied on dose-related methacholine (MeCh 2, 3, and 4.5 micrograms i.v.)-induced bronchoconstriction in anaesthetized rats. BM (0.4 or 2 mg kg-1) was given intraperitoneally 24 h before the experiment followed by a similar dose intravenously, 12 min before MeCh challenge. The bronchodilator drugs were given i.v. as acute single doses. BM 0.4 mg kg-1 counteracted significantly MeCh-induced bronchoconstriction without modifying MeCh-induced transient bradycardia and hypotension. BM 2 mg kg-1 failed to improve that response. A time interval of 24 h after pretreatment proved mandatory to produce these effects. Combined treatment with BM 0.4 mg kg-1 + Ter 20 micrograms kg-1 antagonized the MeCh-induced bronchoconstriction in an additive manner at 2 and 3 micrograms of MeCh, but a synergistic interaction was found at the largest MeCh dose. The effects of the other combinations (BM 0.4 mg kg-1 + Theo 20 mg kg-1 and BM 0.4 mg kg-1 + Ipra 0.5 microgram kg-1) on airways failed to exceed the expected sum of the individual drugs. The combination of BM + Ter was selective to the airways only, whereas BM + Theo also counteracted MeCh-induced bradycardia and BM + Ipra counteracted both hypotension and bradycardia. It is concluded that combined treatment with glucocorticoid and beta 2-adrenoceptor agonist may result in a synergistic interaction on severe airway obstruction without significant influence on cardiovascular system.

Animals↗

PubMed1985

The effect of prednisolone and ketotifen on the antigen-induced bronchoconstriction and mediator release in rat isolated lungs.

Using a new method for inducing IgE-mediated, systemic anaphylaxis in the rat both prednisolone and ketotifen had been shown previously to be effective in suppressing the bronchial anaphylaxis in vivo. In order to study the mode of action underlying their bronchoprotective effect, both agents were also tested on the antigen-induced bronchoconstriction in rat isolated lungs in relation to the mediator release in the lung-effluent. The presence of histamine, 5-hydroxytryptamine (5-HT) and SRS-A could be detected biologically in the lung-effluent during bronchoconstriction. Histamine and 5-HT were determined quantitatively by means of h.p.l.c. with fluorimetric detection, whereas SRS-A was determined using the guinea-pig ileum in a cascade set-up. Although both prednisolone and ketotifen inhibited the antigen-induced bronchoconstriction effectively, it appeared that only prednisolone suppressed the release of histamine, 5-HT and SRS-A in the lung-effluent significantly, whereas ketotifen had no effect. On account of these data it is suggested that the bronchoprotective effect of prednisolone is mainly based on inhibition of the release of the mediators involved, whereas the effect of ketotifen may be based on receptor antagonism.

Anaphylaxis↗

PubMed1983

Effect of physical training on exercise-induced bronchoconstriction.

A 6-week period of physical training of 28 asthmatic children reduced the exercise-induced percentage fall in peak expiratory flow (from baseline) from 44 +/- 4% (mean +/- SE) to 30 +/- 4%. Resting pulmonary function was unchanged. Resting and maximum heart rate (submaximal treadmill running) and postexercise plasma lactate were all lowered by training. The individual values for exercise-induced bronchoconstriction and postexercise plasma lactate correlated positively before and after training. Furthermore, the training-induced reduction in these parameters correlated. In 14 asthmatic children, who served as controls, exercise-induced bronchoconstriction and physical fitness remained unchanged during a comparable period. The study demonstrates a beneficial effect of endurance training on exercise-induced bronchoconstriction and working capacity.

Asthma↗

PubMed1985

Evidence for substance P-immunoreactive spinal afferents that mediate bronchoconstriction.

The origin and functional role of capsaicin-sensitive substance P-(SP-) immunoreactive (IR) nerve fibres in the lower airways were studied in the guinea-pig. Stellatectomy caused a significant reduction of SP-IR in the lung and pulmonary artery. Immunohistochemical analysis, however, did not reveal any clear-cut change in the number and distribution of SP-IR fibres in the lung of these animals. After combined stellatectomy plus local capsaicin treatment of the vagal nerves, most SP-IR nerves disappeared in the lower airways. The bronchoconstriction induced by capsaicin was significantly reduced after stellatectomy and abolished after stellatectomy plus capsaicin pretreatment of the vagal nerves. Ether inhalation caused bronchoconstriction, which was not influenced by stellatectomy but markedly reduced by combined capsaicin treatment of vagal nerves and stellatectomy. Stellate ganglion stimulation in animals that had been chemically sympathectomized by 6-OH-dopamine caused bronchoconstriction, which was resistant to cholinergic or adrenergic receptor blockade. This response was absent after systemic capsaicin pretreatment, suggesting that it was due to antidromic stimulation of afferent fibres traversing the stellate ganglion. In conclusion, the present data suggest that the lower airways receive SP-IR capsaicin-sensitive C-fibre afferents of both vagal and spinal origin. These sensory fibres seem to have branches both within the bronchial smooth muscle and around blood vessels.

Afferent Pathways↗

PubMed1972

Metabolic changes preceding exercise-induced bronchoconstriction.

Five asthmatics aged 25-30 were studied during bicycle ergometer and treadmill exercise. Metabolic and ventilatory changes during exercise were compared with the degree of bronchoconstriction which followed exercise. In all patients bronchoconstriction was greater after treadmill exercise. Contrary to previous suggestions, exercise-induced bronchoconstriction did not seem to be caused by lactic acidosis, increase in minute ventilation, acidaemia, hypocapnia, or change in arterial Po(2)

Acidosis↗

PubMed1975

Atropine, sodium cromoglycate, and thymoxamine in PGF2 alpha-induced bronchoconstriction in extrinsic asthma.

In six patients with extrinsic bronchial asthma the inhalation of prostaglandin (PG) F2 alpha in a small dosage produced significant bronchoconstriction, whereas PGE2 produced bronchodilatation. In these patients cholinergic blockade with atropine partially inhibited the PGF2 alpha-induced bronchoconstriction, but the alpha-receptor-blocking drug thymoxamine and sodium cromoglycate did not. These results suggest that the effect of PGF2 alpha is mediated through cholinergic receptors in the airways, and this effect is grossly exaggerated in asthma. The failure to inhibit PGF2 alpha-induced bronchoconstriction with sodium cromoglycate and the observation of an inhibitory effect of sodium cromoglycate in both allergic and exercise asthma suggest that locally formed PGF2 alpha may not be the main factor in the pathogenesis of bronchial asthma.

Adolescent↗

PubMed1985

Plasma histamine concentration during propranolol induced bronchoconstriction.

The mechanism of propranolol induced bronchoconstriction in asthma is uncertain, as airway beta adrenoceptors are not innervated by sympathetic nerves and circulating adrenaline concentrations are not raised. Propranolol 10 mg was infused over 27 minutes in 14 subjects with mild asthma. Peak expiratory flow (PEF) decreased by 80-235 l/min (17-51% of baseline) in nine subjects, who were called "responders," and by less than 50 l/min (12% of baseline) in five "non-responders". These two groups did not differ in baseline ventilatory function or in any clinical characteristic. In "responders" mean PEF had decreased significantly from 440 to 390 l/min after infusion of propranolol 2.1 mg, though the maximum fall in PEF occurred during or within five minutes of the end of the infusion. In nine of the subjects (six "responders" and three "non-responders") the possibility that propranolol induced bronchoconstriction is due to blockade of mast cell beta receptors leading to increased mediator release was examined by measurement of plasma histamine concentration as an index of mast cell degranulation. There was no consistent change in plasma histamine concentration in either group. No evidence of increased mast cell mediator release has been found in association with propranolol induced bronchoconstriction.

Adult↗

PubMed1986

Effect of verapamil and sodium cromoglycate on leukotriene D4 induced bronchoconstriction in patients with asthma.

Leukotriene D4 (LTD4) may be an important mediator in asthma. The effect of verapamil and sodium cromoglycate on LTD4 induced bronchoconstriction has been examined in seven patients with asthma. The bronchoconstrictor response to increasing concentrations of inhaled LTD4 (0.0032-50 micrograms/ml) was assessed by measuring changes in FEV1, specific airways conductance, and flow rate at 30% of vital capacity (V30(p)). Results were expressed as the provocation concentration (PC) producing a 10% fall in FEV1 (PC10FEV1), a 35% fall in specific airways conductance (PC35SGaw), and a 30% fall in flow at 30% of vital capacity (PC30 V30(p)). Neither verapamil nor cromoglycate inhibited LTD4 induced bronchoconstriction in asthmatic subjects. These results suggest that in asthmatic patients LTD4 induced bronchoconstriction is not mediated via verapamil or cromoglycate sensitive mechanisms.

Adult↗

PubMed1989

Effects of salbutamol on bronchoconstriction, bronchial hyperresponsiveness, and leucocyte responses induced by platelet activating factor in man.

Platelet activating factor, a potent mediator of inflammation, causes a sustained increase in airway responsiveness to methacholine in man and has been implicated in asthma. The effect of the beta 2 agonist salbutamol (200 micrograms by inhalation) on platelet activating factor induced bronchoconstriction and airway hyperresponsiveness was studied in seven normal subjects in a double blind, crossover study. Salbutamol only partially inhibited the platelet activating factor induced fall in partial flow at 30% of vital capacity (Vp30) (mean percentage fall 47.6 (SEM 7.9); p less than 0.001), whereas it completely blocked a similar degree of bronchoconstriction induced by methacholine. Salbutamol did not prevent the accompanying transient flushing and chest irritation and did not affect the transient neutropenia (mean % fall 69.5 (13.6); p less than 0.01) or the rebound neutrophilia (mean % increase 84.7 (24.7); p less than 0.05) that followed platelet activating factor. There was an increase in the airway responsiveness to methacholine following inhalation of platelet activating factor, the maximum mean change being a three fold increase in PC40 (the provocative concentration of methacholine causing a 40% fall in Vp30) on day 3 (p less than 0.01). Salbutamol caused a significant attenuation of this response on day 3 (p less than 0.02) but had no significant effect on days 1 and 7. Thus a therapeutic dose of salbutamol caused partial inhibition of platelet activating factor induced bronchoconstriction and had a minimal effect on the increased bronchial responsiveness following platelet activating factor.

Adult↗

PubMed1981

The mechanism of the bronchoconstriction induced by unilateral orthodromic stimulation of the carotid sinus nerves.

Unilateral stimulation of carotid sinus nerve afferents at 2 and 4 V produced pulse duration-dependent reflex bronchoconstriction which was unaffected by midcervical, bilateral vagotomy. The bronchoconstriction consisted of two pharmacologically distinct components. One component was blocked by atropine or atropine methiodide, and other was blocked by either mepyramine or disodium cromoglycate. Combinations of atropine or atropine methiodide with mepyramine or disodium cromoglycate completely eliminated bronchoconstrictor responses to nerve stimulation. These data indicate that two separate bronchoconstrictor reflexes, possibly resembling serotonin- and diazoxide-induced reflex bronchoconstriction are activated by stimulation of afferent fibers in the carotid sinus nerves.

Airway Resistance↗

PubMed1982

Dose-dependent inhibition of cold air-induced bronchoconstriction by atropine.

We undertook a study to demonstrate whether inhalation of atropine could inhibit cold air-induced bronchoconstriction in a dose-dependent fashion. In seven subjects with asthma we assessed the effects of placebo and of various doses of inhaled atropine (0.13-2.08 mg) on a base-line specific airway resistance (sRaw) and on the increase in sRaw produced by 5 min of voluntary eucapnic hyperventilation with subfreezing air at -17 degrees C. We also assessed the effect of the lowest doses of atropine on the increase in sRaw produced by five breaths of 1.0% metacholine. Atropine in doses of 0.13 or 0.26 mg caused a maximal reduction in base-line sRaw and completely inhibited the effect of 1.0% methacholine on sRaw, but it did not inhibit the bronchomotor response to cold air. Higher doses of atropine did inhibit the effect of cold air on sRaw in a dose-dependent fashion. The dose of atropine required to inhibit this effect of cold air varied with the increase in sRaw produced by cold air after placebo. These results suggest that cold air causes bronchoconstriction through vagal pathways and that higher doses of antimuscarinic agents are required to inhibit vagally mediated bronchoconstriction than those required to reduce base-line airway tone or to inhibit the effects of a large dose of an inhaled muscarinic agonist.

Adult↗

PubMed1984

Massive postmortem bronchoconstriction in guinea pig lungs.

A special phenomenon (difficult to inflate and deflate) occurring in the postmortem guinea pig lungs was studied in 40 animals. Thirty minutes after excision of the lungs or exsanguination, less than 50% of the lungs could be inflated even at high inflation pressure (34 cmH2O), and most gas was trapped during deflation. The amount of trapped gas volume at 30 min was related to the degree of lung inflation maintained during the 5- to 30-min period after exsanguination. Since stiffness of the lung tissue was unlikely to explain the phenomenon, we speculated airway obstruction as the major factor. No foam or bubbles were found in larger airways and we thus hypothesized that the obstruction was due to bronchoconstriction. This was confirmed histologically in that the lumina of both bronchi and bronchioles were constricted. The latent period to the onset of this constriction was short (approximately 5 min). It was not associated with O2 availability but was delayed an additional 15 min by a thromboxane inhibitor (dazoxiben). Neither maintaining lung temperature at 37 degrees C nor vagotomy and/or cervical transection prevented the constriction. Without exsanguination, onset of bronchoconstriction was delayed by about 1 h. We conclude that postmortem bronchoconstriction may be caused by release of an endogenous constrictor agent.

Airway Obstruction↗

PubMed1984

Cigarette smoke-induced bronchoconstriction in dogs: vagal and extravagal mechanisms.

We reassessed the severity of cigarette smoke-induced bronchoconstriction and the mechanisms involved in anesthetized dogs. To evaluate the severity of smoke-induced bronchoconstriction, we measured airway pressure and airflow resistance (Rrs, forced oscillation method). We studied the mechanisms in other dogs by measuring airway pressure, central airway smooth muscle tone in tracheal segments in situ, and respiratory center drive by monitoring phrenic motor nerve output, including the role of vagal and extravagal nerves vs. the role of blood-borne materials during inhalation of cigarette smoke. Rrs increased more than fourfold with smoke from one cigarette delivered in two tidal volumes. About half the airway response was due to local effects of smoke in the lungs. The remainder was due to stimulation of the respiratory center, which activated vagal motor efferents to the airway smooth muscle. Of this central stimulation, about half was due to blood-borne materials and the rest to vagal pulmonary afferents from the lungs. We conclude that inhalation of cigarette smoke in dogs causes severe bronchoconstriction which is mediated mainly by extravagal mechanisms.

Airway Resistance↗

PubMed1985

Bronchoconstriction in asthmatics exposed to sulfur dioxide during repeated exercise.

Young male volunteers with mild asthma and hypersensitivity to methacholine were exposed for 75 min with natural breathing to 0.0, 0.25, 0.5, and 1.0 ppm SO2. Each exposure included three 10-min periods of moderate treadmill exercise (minute ventilation 21 l . m-2 . min-1, O2 consumption 25 ml . kg-1, and heart rate 120/min). Specific airway resistance (sRaw) was not significantly increased after exercise in 0.25 ppm SO2, relative to the control exposure (clean air). In 0.5 and 1.0 ppm SO2, sRaw was increased twofold and threefold above preexposure levels, respectively, corresponding to increases of 3.2 and 9.2 cmH2O . s in excess over the increases seen in clean air (P less than 0.001). There was a broad range of responses to exercise and SO2. The increases in sRaw after the second and third exercises were significantly less than after the first exercise. Respiratory impedance measured by forced random noise suggests that the induced bronchoconstriction was primarily associated with peripheral airways. These results confirm that mild asthmatics selected for methacholine sensitivity have as a group significant bronchoconstriction in response to short-term moderate exercise with natural breathing in 1.0 and 0.5 ppm SO2. In addition, the induced bronchoconstriction is decreased after short-term repeated exercise in SO2.

Adult↗