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PubMed1987

Effects of bronchoconstriction on respiratory muscle activity during expiration.

The effect of methacholine-induced bronchoconstriction on the electrical activity of respiratory muscles during expiration was studied in 12 anesthetized spontaneously breathing dogs. Before and after aerosols of methacholine, diaphragm, parasternal intercostal, internal intercostal, and external oblique electromyograms were recorded during 100% O2 breathing and CO2 rebreathing. While breathing 100% O2, five dogs showed prolonged electrical activity of the diaphragm and parasternal intercostals in early expiration, postinspiratory inspiratory activity (PIIA). Aerosols of methacholine increased pulmonary resistance, decreased tidal volume, and elevated arterial PCO2. During bronchoconstriction, when PCO2 was varied by CO2 rebreathing, PIIA was shorter at low levels of PCO2, and external oblique and internal intercostal were higher at all levels of PCO2. Vagotomy shortened PIIA in dogs with prolonged PIIA. After vagotomy, methacholine had no effects on PIIA but continued to increase external oblique and internal intercostal activity at all levels of PCO2. These findings indicate that bronchoconstriction influences PIIA through a vagal reflex but augments expiratory activity, at least in part, by extravagal mechanisms.

Animals↗

PubMed1987

Cold-induced bronchoconstriction: role of cutaneous reflexes vs. direct airway effects.

To determine the relative contributions of direct airway vs. reflex cutaneous thermal receptor stimulation in cold-induced bronchoconstriction, we isolated these two aspects of cold exposure in 10 asthmatics and 13 normal subjects. Ice packs were applied to the skin of the face, chest, thigh, and upper arm in random sequence while serially measuring specific conductance. In this fashion a limited mapping of skin-mediated bronchoconstriction was established. Warm packs were applied to the same areas of control for any potential nonspecific stimulatory effects. Cooling the skin induced bronchoconstriction to a similar degree in both groups; this effect was very small, did not induce symptoms, and was only seen with stimulation of the face. At another time, the subjects performed isocapnic hyperventilation of frigid air to ascertain their response to direct airway cooling. A moderate but significant correlation existed between skin and airway sensitivity; however, the magnitude of the two responses differed markedly. Breathing cold air at rest had no effect on lung function; however, elevating ventilation promptly produced bronchial narrowing. Hence, in a cold environment, the most potent stimulus for the development of airway obstruction in asthmatics derives from a direct airway effect.

Adult↗

PubMed1988

Bronchoconstriction elicited by isocapnic hyperpnea in guinea pigs.

We demonstrated spontaneous self-limited bronchoconstriction after eucapnic dry gas hyperpnea in 22 anesthetized, mechanically ventilated guinea pigs pretreated with propranolol (1 mg/kg iv). Eucapnic hyperpnea "challenges" of room temperature dry or humidified gas (5% CO2-95% O2) were performed by mechanically ventilating animals (150 breaths/min, 3-6 ml tidal volume) for 5 min. During a "recovery" period after hyperpnea, animals were returned to standard ventilation conditions (6 ml/kg, 60 breaths/min, 50% O2 in air, fully saturated at room temperature). After dry gas hyperpnea (5 ml, 150 breaths/min), respiratory system resistance (Rrs) increased in the recovery period by 7.7-fold and dynamic compliance (Cdyn) decreased by 79.7%; changes were maximal at approximately 3 min posthyperpnea and spontaneously returned to base line in 10-40 min. This response was markedly attenuated by humidification of inspired air. Four consecutive identical dry air challenges resulted in similar posthyperpnea responses in four animals. Increasing the minute ventilation during hyperpnea (by varying tidal volume from 3 to 6 ml) caused increased bronchoconstriction in a dose-dependent fashion in six animals. Neither vagotomy nor atropine altered the airway response to dry gas hyperpnea. We conclude that dry gas hyperpnea in anesthetized guinea pigs results in a bronchoconstrictor response that shares five similar features with hyperpnea-induced bronchoconstriction in human asthma: 1) time course of onset and spontaneous resolution, 2) diminution with humidification of inspired gas, 3) reproducibility on consecutive identical challenges, 4) stimulus-response relationship with minute ventilation during hyperpnea, and 5) independence of parasympathetic neurotransmission.

Airway Resistance↗

PubMed1989

Effect of a thromboxane receptor antagonist on PGD2- and allergen-induced bronchoconstriction.

In this study we investigated the effect of the selective and potent thromboxane A2 (TxA2) receptor antagonist GR32191 on smooth muscle contraction induced by the TxA2 analogue U46619, prostaglandin (PG) D2, PGF2 alpha, and methacholine (MCh) in guinea pig airways in vitro and the airways response provoked by inhaled PGD2 and MCh in asthmatic subjects in vivo. GR32191 antagonized competitively the contractile responses of all three prostanoids to a similar degree but had no effect on MCh-induced contractions. In asthmatic subjects GR32191, in a single oral dose of 80 mg, did not affect base-line airway caliber or MCh-induced broncho-constriction but caused significant inhibition of PGD2-induced bronchoconstriction, displacing the concentration-response curves to the right by greater than 10-fold. The effect of the same oral dose of GR32191 on allergen-induced immediate bronchoconstriction was subsequently investigated in allergic asthmatic subjects. In individual subjects, GR32191 inhibited to varying degrees the overall bronchoconstrictor response, with the maximum effect occurring between 10 and 30 min after allergen challenge. These studies suggest that prostanoids contribute to the immediate bronchoconstriction induced by inhaled allergen in allergic asthmatics, and that this effect is mediated by stimulation of a thromboxane receptor.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1990

Oxygen radicals in capsaicin-induced bronchoconstriction.

The role of oxygen radicals in capsaicin-induced bronchoconstriction was investigated using scavengers of the radicals. A total of 48 guinea pigs weighing 293 +/- 7 g were employed in this study, which consisted of two phases. In phase 1, 35 anesthetized paralyzed animals were divided into five groups: group 1A, control (n = 6); group 1B, chronic dimethylthiourea (DMTU, n = 12); group 1C, acute DMTU (n = 6); group 1D, superoxide dismutase (n = 4); and group 1E, catalase (n = 7). All animals were injected with capsaicin (16 micrograms/kg iv), and changes in respiratory compliance and maximal expiratory flow rate were used as indicators of bronchoconstriction. The capsaicin injection caused a marked airway spasm that was significantly ameliorated by chronic DMTU pretreatment, but no amelioration was noted with the other treatments. An additional study for group 1C was performed using a double dose of DMTU. Again no amelioration was found. In phase 2, 13 animals were divided into two groups: group 2A, substance P (SP, n = 7) and group 2B, chronic DMTU + SP (n = 6). There was no significant difference in SP-induced bronchoconstriction between animals in these two groups. These data suggest that capsaicin-induced airway constriction is modulated by oxygen radicals which may augment mainly on the biosynthesis and/or axonal transport of tachykinins.

Animals↗

PubMed1990

Increased leukotriene E4 excretion during antigen-induced bronchoconstriction in allergic sheep.

The metabolism of leukotrienes (LT) in the sheep was investigated to define markers of 5-lipoxygenase involvement in allergic responses, obtainable by noninvasive techniques. Intravenous administration of 14, 15-[3H]LTC4 (0.5 microCi/kg) revealed a rapid clearance from the circulation (half time = 90 s). Circulatory metabolism was apparent, with early formation (within 1 min) of LTD4 and LTE4 shown by reverse-phase high-pressure liquid chromatography (RP-HPLC). Urinary 3H excretion comprised 10% of the original dose. [3H]LTE4 (characterized by coelution with authentic standards during RP-HPLC analysis) was observed in early urine samples. By use of a sensitive and specific RP-HPLC radioimmunoassay analysis, immunoreactive material coeluting with LTE4 was detected in urine from allergic sheep. Excretion of this material was significantly increased during antigen-induced acute bronchoconstriction in eight conscious allergic sheep [preantigen, 65.70 +/- 24.27 (SE) pg; 0-1 h postantigen, 208.00 +/- 71.10 pg, P less than 0.05], but not during late responses. However, total postantigen LTE4 excretion (37.8 - 956.1 pg/8 h) was highly correlated (r = 0.976, P less than 0.001) with the severity of bronchoconstriction (445.3 - 2,409.1% specific pulmonary resistance per hour) assessed by measurement of the area under the curve of pulmonary function plotted against time. These findings represent an important demonstration of in vivo allergen-induced peptide LT generation in a physiologically characterized animal model of prolonged allergic bronchoconstriction and further substantiate an important role for LT in this model of allergic asthma.

Animals↗

PubMed1990

Capsaicin-induced bronchoconstriction and neuropeptide release in guinea pig perfused lungs.

In the guinea pig isolated perfused lung, we have examined the relationship between the effects of capsaicin and neuropeptide release and the possible existence of an axon reflex arrangement. Bolus injections into the pulmonary artery of capsaicin (1-100 pmol), substance P (10-1,000 pmol), and neurokinin (NK) A (10-100 pmol) produced a concentration-dependent bronchoconstriction, whereas calcitonin gene-related peptide (CGRP, 20-40 nmol) was without effect. Repeated administration of capsaicin at 40- to 60-min intervals was not associated with tachyphylaxis. These data support the presence of a NK2- (or NKA) type of tachykinin receptor in the guinea pig airways. Tetrodotoxin (0.3-3 microM) inhibited the effect of capsaicin, indicating that an axon reflex was operant. Capsaicin increased overflow of CGRP-like immunoreactivity (-LI) and NKA-LI, the latter only during concurrent infusion of the enkephalinase inhibitor phosphoramidon (3 microM). Phosphoramidon also increased overflow of CGRP-LI, suggesting that both NKA and CGRP were catabolized by a similar enzyme. The purine nucleoside adenosine did not cause any detectable overflow of CGRP-LI, indicating that neuropeptides may not be involved in adenosine-evoked bronchoconstriction and that bronchoconstriction per se does not induce neuropeptide overflow. Capsaicin and NKA had only minor effects on buffer flow, whereas substance P produced pulmonary vasoconstriction. These data clearly demonstrate that capsaicin acts via an axon reflex in the guinea pig airways. Supramaximal concentrations of capsaicin are needed to detect neuropeptide overflow, but the possibility exists that released neuropeptides mediate its effects.

Acetylcholine↗

PubMed1993

Expiratory airflow limitation and hyperinflation during methacholine-induced bronchoconstriction.

To investigate the role of airflow limitation on the increase of end-expiratory lung volume (EELV) during bronchoconstriction, nine stable asthmatic subjects and seven healthy subjects were challenged with inhaled methacholine (MCh). Changes in airway caliber were assessed by using forced expiratory volume in 1 s, partial forced expiratory flow at 50% of control forced vital capacity, and specific airway conductance. To detect airflow limitation, tidal flow-volume curves were superimposed on partial forced flow-volume curves at absolute lung volume. The electromyogram of the diaphragm was recorded by surface electrodes in four asthmatic and four healthy subjects, and the electrical diaphragmatic activity (DIA) during expiration was expressed as a percentage of the duration of expiratory time. In 10 subjects (9 asthmatic and 1 healthy) the partial forced expiratory flow recorded after some MCh dose impinged on tidal expiratory flow recorded before MCh. When this occurred it was associated with an increase in EELV by 0.54 +/- 0.07 (SE) liter (P < 0.001), which was larger than that occurring when lower MCh doses (0.11 +/- 0.04 liter, P < 0.05) were used, and with a moderate increase in DIA of 15 +/- 2.5% (P < 0.01). Six healthy subjects did not increase EELV after MCh despite a significant degree of bronchoconstriction; in these subjects tidal expiratory flow never impinged on forced expiratory flow, and DIA never increased. These results suggest that hyperinflation during MCh-induced bronchoconstriction is triggered by dynamic compression of the airways and is associated with moderate increase of DIA during expiration.

Adolescent↗

PubMed1981

Effect of intravenous histamine, allergen (Ascaris suum Extract) and compound 48/80 and inhaled allergen-aerosol on bronchoconstriction and histamine release.

The effect of a histamine releaser (48/80), an antigen (Ascaris suum extract) and of exogenous histamine infusion on antigen aerosol-induced bronchoconstriction was investigated in 24 mongrel dogs. During these substance infusions, the high values of arterial plasma histamine did not correlate with the degree of bronchoconstriction. Further, a severe bronchoconstriction with a relatively low arterial plasma histamine concentration was observed during antigen inhalation. During substance inhalation, a high local concentration of histamine is assumed to explain the increased bronchial "sensitivity" to actual plasma levels of histamine. Also, the responsiveness of the bronchial tree to antigen aerosol was observed to be reduced 90 min after induction of a strong histamine release. The importance of histamine in the first phase of immediate hypersensitivity is discussed.

Allergens↗

PubMed1985

Ventilatory inhomogeneity associated with acute bronchoconstriction in asthmatic patients.

Ventilation inhomogeneity was assessed in asthmatic subjects before and after antigen-induced bronchoconstriction and bronchodilator administration. As an index of inhomogeneous distribution of inspired air, the mean dilution number (the ratio of the first to zero moments) was calculated from each multibreath nitrogen washout during spontaneous breathing. This index was compared to plethysmographic, spirometric, and lung volume indices. In the baseline state, a weak relationship existed between the mean dilution number (MDN) and indices of mechanical abnormality, FEV1/FVC and SRAW. Antigen-induced bronchoconstriction led to increases in the MDN, SRAW, and RV/TLC, and a decrease in FEV1/FVC. The reverse effects were found by administering bronchodilators. No statistically significant correlations were found between changes in MDN and changes in the other indices of pulmonary function. Thus, the maldistribution of inspired air resulting from acute bronchoconstriction cannot be quantified from common indices of pulmonary function.

Adult↗

PubMed1986

Inhibition of acetylcholine-induced bronchoconstriction in asthmatics by nifedipine.

The calcium-dependent constriction of bronchial smooth muscle cells and release of mediators derived from mast cells is important in the pathophysiology of asthma. We hypothesized that nifedipine, a slow calcium channel blocker, would inhibit or attenuate acetylcholine-induced bronchoconstriction in asthmatics. Because one consequence of mast cell activation is the release of platelet-activating factor, we wondered whether thromboxane levels would be increased during acute bronchial constriction in asthmatics. Bronchoconstriction was induced in 8 asthmatics (6 men, 2 women) by acetylcholine; each subject was pretreated either with placebo or nifedipine (20 mg sublingually) on 2 separate days. Vital capacity, forced expiratory volume in 1 s, peak expiratory flow rates and oscillatory resistance were measured prior to and after the intake of placebo or nifedipine as well as after an acetylcholine challenge. Pretreatment with nifedipine significantly attenuated acetylcholine-induced changes in all four lung function parameters studied, but did not significantly influence the increase in thromboxane B2 plasma concentrations observed after the acetylcholine challenge. From these data we conclude that nifedipine inhibits the acetylcholine-induced bronchoconstriction in asthmatics. This effect may be either a direct action on bronchial smooth muscle or may be due to the inhibition of mediators other than thromboxane.

Acetylcholine↗

PubMed1985

Inhibition by amoxanox (AA-673) of the immunologically, leukotriene D4- or platelet-activating factor-stimulated bronchoconstriction in guinea pigs and rats.

We studied the effects of amoxanox (AA-673) on allergic asthma and spasmogen-induced bronchoconstriction in guinea pigs and rats. Amoxanox given orally or parenterally inhibited allergic asthma mediated by IgE, IgG1, or heterologous IgG in guinea pigs and by IgE in rats. This compound also reduced leukotriene D4- and platelet-activating factor-induced bronchoconstriction in guinea pigs, strongly suggesting an antagonistic activity against slow reacting substance of anaphylaxis (SRS-A). Histamine- or acetylcholine-induced bronchoconstriction was not significantly affected by amoxanox. These antiasthmatic effects of amoxanox seem to be associated with an inhibition of the release of chemical mediators such as histamine and SRS-A and with an antagonism against SRS-A.

Aminopyridines↗

PubMed1988

Involvement of PAF-acether in anaphylactic bronchoconstriction induced in guinea pigs by aerosolized antigen.

Bronchoconstriction following the aerosolization of PAF-acether or antigen to guinea pigs induces autodesensitization, but the responses to direct spasmogenic substances are not modified. Bronchoconstriction by PAF-acether is not reduced when it is aerosolized to passively sensitized animals previously desensitized by repeated inhalations of the allergen (ovalbumin). In contrast, when passively sensitized animals are initially desensitized to PAF-acether by repeated inhalations of this agonist, ovalbumin aerosolization induces a bronchoconstriction which is significantly reduced when compared with the response obtained in nondesensitized animals though, in this case, the response to aerosolized histamine is not modified. Thus, PAF-acether is released during intrapulmonary anaphylactic shock induced by aerosolized ovalbumin and can be a prime candidate for its development.

Aerosols↗

PubMed1988

Bronchoconstriction induced by platelet-activating factor in the guinea pig and its inhibition by CV-3988, a PAF antagonist: serial changes in findings of lung histology and bronchoalveolar lavage cell population.

Platelet-activating factor (PAF), 1-o-alkyl-2-acetyl-sn-glyceryl-3-phosphoryl choline, induced acute bronchoconstriction in the guinea pig when intravenously administered in a very small dosage (30 ng/kg). Serial changes in findings of lung histology and bronchoalveolar lavage (BAL) cell population were studied. Severe bronchial smooth muscle contraction and hypersecretion were followed by eosinophil infiltration. Increase in the number of eosinophils was also elucidated by BAL. Prominent damage to the ciliated bronchial epithelial cells was suggested from the lung histology, which was also supported by the fact that a number of ciliated cells was recovered by BAL. Late-onset bronchial constriction after PAF infusion was not observed. CV-3988, one of the specific PAF antagonists, completely inhibited the PAF-induced bronchoconstriction when administered before the PAF infusion. We concluded that PAF is a potent in vivo agent which brings about hypersecretion, eosinophil accumulation, bronchial epithelial damage as well as bronchoconstriction in the guinea pig, and that its action is completely blocked by CV-3988.

Animals↗

PubMed1987

Reflex decrease of histamine-induced bronchoconstriction after laryngeal stimulation in humans.

The aim of this work was to determine whether the nonadrenergic, noncholinergic, inhibitory nervous system can be reflexly activated in humans by laryngeal stimulation. The stimulation was achieved with a cytology brush passed through a bronchoscope previously introduced transnasally and positioned just above the epiglottis. In one series of experiments, subjects were premedicated with beta-adrenergic and cholinergic blockers, and bronchoconstriction was induced by histamine inhalation. The results showed that mechanical irritation of the vocal cords with the cytology brush produced a sharp, short-lasting (less than 1 min) decrease in RL from (mean +/- SE) 6.8 +/- 2.1 to 4.8 +/- 1.5 cm H2O.L-1.s, and in the absence of parasympathetic blockade, laryngeal irritation produced a fall in RL from (mean +/- SE) 9.0 +/- 3.7 to 5.4 +/- 2.0 cm H2O.L-1.s (p less than 0.0001) (ANOVA). This decrease in RL was independent of the slight cough produced by laryngeal stimulation and reflects a change in lower and not upper airway resistance. Adequacy of the beta-adrenergic and cholinergic blockade was checked with an intravenous infusion of isoproterenol and inhaled methacholine, respectively. In 2 subjects, the fall in RL was abolished by a block of the superior laryngeal nerves and direct local anesthesia of the vocal cords. We conclude that mechanical irritation of the larynx produces a partial reversal of histamine-induced bronchoconstriction that is mediated through nervous pathways that are neither beta-adrenergic nor cholinergic in origin. We suggest that this decrease in bronchoconstriction is modulated by the nonadrenergic, noncholinergic, inhibitory nervous system.

Adult↗

PubMed1989

Anticholinergic blockade of beta-blocker-induced bronchoconstriction.

The mechanism of propranolol-induced bronchoconstriction (PIB) remains unclear. Previous uncontrolled studies have suggested that atropine antagonizes PIB in asthma. We conducted a randomized, double-blind, placebo-controlled study of the effect of a new anticholinergic agent, oxitropium bromide, on bronchoconstriction induced by inhaled propranolol in seven subjects with mild asthma 24 to 39 yr of age. Inhaled propranolol induced long-lasting reduction in specific airway conductance (SGaw) in all subjects. This was associated with airway beta-adrenoceptor blockade as demonstrated by a shift in the isoproterenol dose-response curve. Propranolol was less potent than methacholine, with a geometric mean dose causing a 35% fall in SGaw of 4.7 mumol for propranolol compared with 0.48 mumol for methacholine. Pretreatment with oxitropium 200 micrograms completely inhibited the fall in SGaw in response to inhaled propranolol in all subjects. Oxitropium also revealed PIB. Cholinergic receptor blockade by oxitropium inhibits bronchoconstriction induced by inhaled propranolol, supporting involvement of cholinergic mechanisms in PIB.

Adult↗

PubMed1990

Effects of humid air breathing during arm or treadmill exercise on exercise-induced bronchoconstriction and refractoriness.

Although it has been reported that inhibitory prostaglandins may be a causal factor in exercise refractoriness, it is still unclear whether exercise-induced bronchoconstriction (EIB) and/or other specific "exercise factors" are necessary to trigger their release and render a subject refractory to subsequent exercise. The purpose of this study was to determine whether non-EIB-producing exercise with the legs or arms could produce refractoriness to a standard treadmill challenge. Eight asthmatic subjects with EIB completed three sessions consisting of two exercise challenges separated by a 30-min rest. In all sessions, the second challenge was done on a treadmill while breathing dry air. Conditions for Challenge 1 were the following: Session A = treadmill, dry air; Session B = treadmill, humid air; Session C = arm cranking, humid air. All three conditions produced a significant degree of refractoriness. There was a tendency for the percent protection index to be greater for Session A; however, no significant differences were found among the three sessions. Therefore, it can be concluded that although both exercise and bronchoconstriction may play a role in producing the refractory period, neither severe bronchoconstriction nor intense exercise with the same muscle groups are required to produce refractoriness.

Adult↗

PubMed1992

Prevention of exercise-induced bronchoconstriction by a new leukotriene antagonist (SK&F 104353). A double-blind study versus disodium cromoglycate and placebo.

The effects of 800 micrograms of inhaled SK&F 104353, a peptidoleukotriene receptor antagonist, and of 20 mg disodium cromoglycate (DSCG) on exercise-induced bronchoconstriction were compared in 18 asthmatic patients. The study was conducted according to a double-blind, crossover, randomized, placebo-controlled design. Two baseline exercise tests were carried out, and pulmonary function tests were done before and at 1, 5, 10, 15, 20, and 30 min after completion of the exercise. Patients showing a 20% or greater decrease in FEV1 in both exercise challenges entered the blinded portion of the study. When placebo was administered before exercise, FEV1 fell to the same extent as during the baseline phase. After SK&F 104353 and DSCG, the bronchoconstriction was attenuated. The mean maximal percentage fall in FEV1 after exercise was 29% after placebo and 20% after SK&F 104353 and DSCG. The differences between the two active treatments did not reach the 5% level of statistical significance, though at 20 min SK&F 104353 showed a more pronounced effect than DSCG. The protective effect suggests an important role of leukotrienes in the pathogenesis of exercise-induced bronchoconstriction.

Adult↗