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PubMed2000

Perception of bronchoconstriction and bronchial hyper-responsiveness in asthma.

The inter-relationship between the perception of bronchoconstriction, bronchial hyper-responsiveness and temporal adaptation in asthma is still a matter of debate. In a total of 52 stable asthmatic patients, 32 without airway obstruction ¿forced expiratory volume in 1 s (FEV(1))/vital capacity (VC) 84.1% (S.D. 7.9%), and 20 with airway obstruction [FEV(1)/VC 60% (4%)], we assessed the perception of bronchoconstriction during methacholine inhalation by using: (i) the slope and intercept of the Borg and VAS (Visual Analog Scale) scores against the decrease in FEV(1), expressed as a percentage of the predicted value; and (ii) the Borg and VAS scores at a 20% decrease in FEV(1) from the lowest post-saline level (PB(20)). Bronchial hyper-responsiveness was assessed as the provocative concentration of methacholine causing a 20% fall in FEV(1) (PC(20)FEV(1)). The reduction in FEV(1) was significantly related to the Borg and VAS scores, with values for the group mean slope and intercept of this relationship of 0.13 (S.D. 0.08) and -1.1 (3.02) for Borg, and 1.5 (1.19) and -12.01 (35) for VAS. PB(20) was 3 (1.75) with Borg scores and 34.6 (20.5) with VAS scores. Compared with the subgroup without airway obstruction, the obstructed subgroup exhibited similar slopes, but lower Borg and VAS intercepts. For similar decreases in FEV(1) (5-20% decreases from the lowest post-saline values), the Borg and VAS scores were lower in the non-obstructed than in the obstructed subgroup. PC(20)FEV(1) was significantly related to both Borg PB(20) and VAS PB(20) when considering all patients. When assessing the subgroups, PC(20)FEV(1) was related to Borg PB(20) and VAS PB(20) in the non-obstructed subjects, but not in the obstructed subjects. In neither subgroup was the log of the cumulative dose related to the Borg and VAS scores at the end of the test. We conclude that, unlike in previous studies, the ability to perceive acute bronchoconstriction may be reduced as background airflow obstruction increases in asthma. Bronchial hyper-responsiveness did not play a major role in perceived breathlessness in patients without airway obstruction, and even less of a role in patients with obstruction. The cumulative dose of agonist did not appear to influence the perception of bronchoconstriction.

Adolescent↗

PubMed1990

[Contribution of the vagal nerve on histamine-induced bronchoconstriction in guinea-pigs].

Recently, it has been suggested that the peripheral vagal nerve might participate in the bronchoconstriction locally in addition to the concept of "vagal reflex". We investigated the contribution of the vagal nerve on the modulation of airway responses to histamine (8 micrograms/kg, iv) in anesthetized and mechanically ventilated guinea-pigs. Airway responses were assessed by measurement of pulmonary resistance (RL). To determine whether the vagal nerve mediates excitatory effects by "vagal reflex" in guinea-pigs, we investigated the effects of vagotomy or hexamethonium (2 mg/kg, iv). Increase in RL induced by histamine was significantly enhanced after the vagotomy or the treatment of hexamethonium. Histamine-induced bronchoconstriction was also enhanced by the vagotomy in the animals after the administration of propranolol (1 mg/kg, iv). To determine whether the peripheral vagal nerve may play any role in the vagotomized animals, we investigated the effect of atropine (1 mg/kg, iv). Atropine reduced histamine-induced bronchoconstriction significantly in the vagotomized guinea-pigs or in the animals treated with hexamethonium. We conclude that the vagal nerve mainly exerts on inhibitory role through the central nervous system, and that the peripheral vagal nerve distal to ganglion plays an excitatory effects by releasing acetylcholine from the terminals in histamine-induced bronchoconstriction in guinea-pigs.

Animals↗

PubMedDate not supplied

Role of chemical mediators in bronchoconstriction induced by kerosene.

Kerosene is a by product of petroleum used in some countries for cleaning, lighting and cooking purposes. Rodriguez de la Vega et al (1981) have presented evidences of the relation between bronchial asthma and the manipulation of kerosene. Since the experiments performed by our group showed that the acute inhalation of the aerosol of kerosene induces bronchoconstriction in rabbits (Casacó et al 1982), we investigated its effect on guinea pig respiratory physiology. In order to elucidate the implication of histamine and arachidonic acid metabolites in kerosene induced bronchoconstriction, we investigated the influence of the administration to guinea pig of a single dose of the histamine H1 antagonist mepyramine (0.1 mg/kg i.v.) 10 minutes before the aerosol and also the effect of the steroidal antinflammatory drug triamcinolone in rabbits (5 mg/kg i.m.) daily during 4 days before the inhalation of kerosene. The histamine concentrations in guinea pig blood before and after the aerosol were also compared. The inhalation of kerosene during 5 min. (20.4 mg/L) by guinea pigs resulted in an increase of airway resistance without increase of blood histamine concentration. On the other hand, the bronchoconstrictive effect of kerosene in guinea pigs and rabbits was not modified by the previous treatment with mepyramine or triamcinolone respectively. The results suggest that the acute bronchoconstriction induced by kerosene is mediated neither by stimulation of histamine H1 receptors nor by the release of chemical mediators.

Airway Resistance↗

PubMed1989

[Mechanisms of bronchoconstriction induced by anaphylaxis in sensitized guinea pigs].

Anaphylactic reaction in sensitized guinea pigs is known to induce bronchoconstriction when an adequate amount of antigen is administrated. This phenomenon has been established as a model of bronchial asthma. To evaluate the mechanism of bronchoconstriction in anaphylaxis, we analyzed the change of endobronchial pressure in sensitized guinea pigs. Guinea pigs weighing 300-600 g were actively sensitized by intracutaneously administrated ovalbumin (10 mg). Two weeks later they were anesthetized and mechanically ventilated with a volume type Harvard respirator. Antigen was administrated intravenously and monitoring of endotracheal pressure and systemic blood pressure was performed. Drugs to modify these reactions were administrated intraperitoneally 30 minutes before antigen challenge. In the control group, the endotracheal pressure showed a curve with the first peak between 0.5 and 1.5 minutes after the antigen challenge. When cyclooxygenase inhibitor (indomethacin) was administered before the antigen, the first peak was markedly suppressed. However, the histamine (H1)-receptor blocker did not suppress the first peak. On the other hand when 5-lipoxygenase inhibitor (AA-861) was administered before the antigen, the increase of intratracheal pressure was suppressed between 2 and 4 minutes after the antigen challenge. The above results may suggest that the first peak of intratracheal pressure derives from bronchoconstriction caused by prostaglandins or thromboxanes, and that the increase of intratracheal pressure at between 2 and 4 minutes derives from bronchoconstriction caused by leukotrienes.

Anaphylaxis↗

PubMed1989

The effect of anticholinergic and beta-agonist pretreatment on bronchoconstriction induced by N-formyl-methionyl-leucyl-phenylalanine.

N-Formyl-methionyl-leucyl-phenylalanine (FMLP), an acylated tripeptide bacterial neutrophil chemotactic factor, has been shown to be a bronchoconstrictor by inhalation in man in vivo. It thus has a putative role in the generation of bronchoconstriction associated with bacterial bronchial infection. We have investigated the effect of pretreatment with the anticholinergic agent, ipratropium bromide (IB), and the beta 2-agonist, fenoterol (F), on FMLP-induced bronchoconstriction. Ten non-asthmatic subjects aged 21-28 yrs performed dose-response curves to nebulized FMLP on 3 study days after pretreatment with saline, F or IB. Amongst the 8 subjects who bronchoconstricted by 20% to FMLP there was a significant increase in the provocative concentration causing a 20% fall in forced expiratory volume in one second (FEV1) (PC20FMLP) after both IB and F. F was significantly better than IB. When comparison was made using absolute fall in FEV1 and including all 10 subjects the same results were found. Partial inhibition of FMLP-induced bronchoconstriction by IB suggests that part of the effect of FMLP is vagally mediated. We suggest that F is acting via modulation of FMLP-induced rises in intracellular free calcium.

Adult↗

PubMed1989

Effects of inhaled thiazinamium chloride on histamine-induced and exercise-induced bronchoconstriction.

The protective efficacy of aerosolized thiazinamium chloride (TC) against histamine-induced and exercise-induced bronchoconstriction was evaluated in 15 subjects with stable, mild asthma. Following reproducible bronchoprovocation with these stimuli, each subject underwent randomized, double-blind, crossover pretreatment with single doses of nebulized TC (300, 600, and 900 micrograms), placebo, and an active control drug (metaproterenol or cromolyn), followed by histamine or exercise challenge (two separate protocols). The results indicated that all doses of TC significantly blocked histamine-induced bronchoconstriction as compared with placebo. Overall, aerosolized TC was ineffective in blocking exercise-induced bronchoconstriction, although 900 micrograms TC tended to be more effective than placebo. Thiazinamium (900 micrograms) produced a modest bronchodilator effect. No clinically significant adverse effects related to TC occurred. We conclude that aerosolized TC is effective in attenuating histamine-induced but not exercise-induced bronchoconstriction in the doses studied. Further studies are warranted to evaluate the role of TC in asthma therapy.

Adult↗

PubMed1989

Reversibility of induced bronchoconstriction by deep inspiration in asthmatic and normal subjects.

Five normal and five asthmatic subjects underwent a progressive methacholine provocation study. At each concentration inspiratory pulmonary resistance (RL) was measured, as well as isovolumic maximal flow and residual volume from both partial and complete forced expirations. Results were compared over the RL range of 6-11 cmH2O.1-1.S-1. The reversibility of bronchoconstriction by deep inspiration was quantified as the ratio of the flow increase to potential maximal increase; the reversibility of gas trapping was the ratio of decrease in residual volume to potential maximal decrease. The reversibility of bronchoconstriction did not differ between the groups. In contrast, the reversibility of gas trapping was smaller in asthmatic subjects (21 +/- 17%) than in normals (84 +/- 6%). As gas trapping reflects airway closure, our findings suggest that during induced bronchoconstriction airway closure is more resistant to the effects of deep inspiration in asthmatic than in normal subjects but the reversibility of bronchoconstriction by deep inspiration is not different.

Adult↗

PubMed1986

Effects of SK&F 93944 (Temelastine), a potent histamine H1-receptor antagonist in pharmacologic and antigen-induced bronchoconstriction.

SK&F 93944, a previously reported non-sedating histamine H1-receptor antagonist, was evaluated for its ability to block pharmacologic-and antigen-induced bronchoconstriction. In the isolated guinea pig trachea, SK&F 93944 (10(-9)-10(-7) M) produced a concentration-dependent inhibition of contractions produced by histamine (pKB = 9.5). Another histamine antagonist, mepyramine (10(-8)-10(-6) M), was less potent (pKB = 8.5). SK&F 93944 (10(-8), 10(-7) M) also significantly depressed the rapid initial phase of antigen-induced contraction of the guinea pig trachea from animals actively sensitized to ovalbumin, while having no effect on the later, more protracted phase of the contractile response. In anesthetized mongrel dogs, selective inhibition of histamine (20 micrograms/kg, i.v.)-induced bronchoconstriction was achieved by SK&F 93944 in doses as low as 30 micrograms/kg, i.v. Terfenadine, a purportedly selective histamine H1-receptor antagonist, blocked both histamine and acetylcholine-induced bronchoconstriction at doses similar to SK&F 93944. In mongrel dogs natively allergic to Ascaris suum antigen, pretreatment with aerosols of either SK&F 93944 or mepyramine (1%; 50 tidal breaths) significantly inhibited bronchospasm elicited by increasing aerosol concentrations of antigen. Thus, SK&F 93944 is a highly potent, selective histamine H1-receptor antagonist which is efficacious vs. pharmacologic and antigen-induced bronchoconstriction.

Animals↗

PubMedDate not supplied

Serum neutrophil chemotactic activity (NCA) during aspirin-induced bronchoconstriction.

In order to determine mast cell involvement in aspirin-induced bronchoconstriction, 16 aspirin-sensitive asthmatics and 18 control patients were studied for serum neutrophil chemotactic activity, using Nelsons method, before and after oral aspirin administration. A significant increase in NCA was observed in 6 aspirin-sensitive asthmatics during aspirin bronchoconstriction. In two persons the increase was lower. In the remaining 8 persons, no increase in NCA was observed during aspirin bronchoconstriction. None of the control patients exhibited an increase in NCA. The authors assume that, in some of the patients with aspirin-induced bronchoconstriction mast cells are really involved.

Adolescent↗

PubMed1987

Cough and bronchoconstriction.

Cough is frequently a symptom in bronchial asthma. Appropriate treatment of asthma is usually associated with a reduction in cough. The relationship between cough and bronchoconstriction is outlined and the role of various airway receptors in the genesis of the two responses is discussed. Experimentally, cough and bronchoconstriction may be separated: inhalations of iso-osmolar aerosols of low chloride ion content appear to be selectively tussigenic and do not cause broncho-constriction. Numerous irritants induce cough and broncho-constriction. Topical lignocaine will abolish cough but has no effect on bronchoconstriction. Beta-agonists and anticholinergic drugs will reduce or prevent bronchoconstriction induced by an irritant and may suppress cough. Cough is mediated by airway receptors and it is possible that broncho-dilating agents act as cough suppressors because they "reset" airway receptors.

Animals↗

PubMed1986

The effect of antigen-induced bronchoconstriction on phrenic nerve activity.

The effects of acute bronchoconstriction, produced by inhalation of Ascaris suum antigen, on both the amplitude and timing of phrenic nerve activity were studied in anesthetized dogs. Blood gas tensions and inspiratory air flow were maintained constant. Bronchoconstriction resulted in a significant increase in the magnitude and rate of rise of the phrenic neurogram during both normal respiratory cycles and cycles when lung inflation was prevented. The increase in the slope of the phrenic neurogram that results from lung inflation was further increased during bronchoconstriction. In addition, in half the animals, there was a significant increase in the tonic phrenic activity measured during expiration. All of these changes were abolished by bilateral cervical vagotomy. Antigen administration did not affect the timing of the different phases of the cycle equally; inspiratory duration was reduced by 51.8% and expiratory duration by 67.6%. Postinspiratory activity of the phrenic (PIIA) was reduced by only 34.7%; thus, during bronchoconstriction PIIA occupied a proportionally greater fraction of the expiratory phase. Vagotomy abolished the changes in respiratory timing and eliminated all PIIA.

Animals↗

PubMed1983

Mediators and reflex bronchoconstriction.

Reflex bronchoconstriction can be induced by mechanical and chemical stimuli to the respiratory tract, especially from the larynx down to the larger intrapulmonary airways. The pathways for these reflexes have been analysed in experimental animals. The afferent nerves include fibres from rapidly adapting ("irritant") receptors in and under the epithelium of the airways, and those from "C-fibre" receptors in the tracheobronchial tree and possible alveoli. Many of the mediators thought to be released in lung antigen antibody reactions and airway tissue damage can be shown to activate these groups of sensory receptors: the mediators include prostaglandins, bradykinin, histamine and 5-hydroxytryptamine. Both the irritant and the C-fibre receptors have been shown to cause reflex bronchoconstriction, as well as other reflex motor actions that influence the diameter of the respiratory tract, such as mucus secretion and laryngeal constriction. They are also responsible for respiratory changes, including coughing. Mediators which are released in bronchial asthma are potential agents in setting up reflex bronchoconstriction. In man the evidence for such a reflex depends primarily on the inhibitory efficiency of atropinic drugs in some forms of asthma. Such evidence cannot be completely unequivocal but, taken with the analogy with animal experiments, there seems to be a prima facie case for reflex bronchoconstriction as one component of the total pattern of an asthma attack.

Animals↗

PubMed1983

Ascaris-induced bronchoconstriction in primates experimentally infected with Ascaris suum ova.

Bronchial provocation with Ascaris allergen evoked bronchoconstriction in home-bred Macaca arctoides monkeys sensitized by experimental infection with embryonated Ascaris suum ova. Inhalation of Ascaris allergen by aerosol prior to infection produced no changes in lung function. In infected animals total lung resistance (RL) increased and dynamic lung compliance (Cdyn) decreased following Ascaris inhalation. The changes in lung function reached a peak, 2-5 min after allergen inhalation, lasted for approximately 30 min and were associated with increases in arterial plasma histamine levels and decreases in arterial Po2 levels. Reproducible changes in lung function were obtained when the monkeys were challenged at bi-weekly intervals and lung sensitivity to Ascaris was maintained for at least 6 months. Histamine produced similar changes in RL and Cdyn before and after infection. Ascaris-induced bronchoconstriction was reversed by the beta 2-stimulant, salbutamol, and was partially reversed by cholinergic blockade with atropine. The responses were not inhibited by antihistamines or sodium cromoglycate although a new anti-allergic agent, FPL 58668 (disodium salt), inhibited Ascaris-induced bronchoconstriction and the increase in plasma histamine levels seen after Ascaris inhalation. Ascaris-induced bronchoconstriction in experimentally infected monkeys provides an animal model demonstrating many of the characteristics of allergic asthma in man and does not require the use of wild-caught monkeys.

Airway Resistance↗

PubMed1978

Anaphylactic bronchoconstriction in rats immunized with antigen-coated latex particles.

Studies have been carried out on the immunization of rats with antigen-coated latex particles. These studies confirmed that a significant lung blood eosinophilia is induced by a repeat intravenous injection of antigen-coated latex particles. Rats treated with antigen-coated latex particles also become sensitive to antigen such that on antigen challenge the animals show bronchoconstriction. Studies show that the bronchoconstriction is specific for antigen, but is unlikely to be mediated by tissue-fixing antibodies. Experiments comparing different immunization schedules involving latex particles indicate a strong association between the level of eosinophilia and degree of antigen-induced bronchoconstriction. These studies suggest that eosinophils may contribute to the anaphylactic bronchoconstriction.

Anaphylaxis↗

PubMed1984

Preventive and reverse effects of nifedipine on human bronchoconstriction "in vitro".

The effects of nifedipine, a calcium channel blocking agent, on human bronchoconstriction induced by acetylcholine and histamine were studied in vitro. Bronchial preparations were obtained from 13 patients undergoing surgery for bronchial carcinoma. Bronchial strips were mounted for continuous isometric tension recording. Acetylcholine and histamine caused bronchoconstrictions, but the constrictive effects were inhibited by 2.9 X 10(-6) M nifedipine. At a concentration of 2.9 X 10(-6) M nifedipine increased by 22-fold the concentration of acetylcholine required to produce a 50% of maximal contraction of bronchial strips, and by 160-fold the concentration of histamine required. Nifedipine also reversed already established bronchoconstrictions by acetylcholine and histamine. The percentage of contraction at 20 min after 2.9 X 10(-6) M nifedipine was 7 +/- 11.1% (mean +/- SEM) and - 21 +/- 20.0% of the control maximal response by 10(-3) M acetylcholine and 10(-3) M histamine, respectively. Thus, nifedipine clearly prevented and reversed pharmacologically-induced bronchoconstriction in humans. These results suggest that it is valuable to administer nifedipine to prevent and treat asthma attack.

Acetylcholine↗

PubMed2001

Secretory leukocyte protease inhibitor, but not alpha-1 protease inhibitor, blocks tryptase-induced bronchoconstriction.

Alpha-1-protease inhibitor (alpha(1)-PI) and secretory leukocyte protease inhibitor (SLPI) are two natural airway serine protease inhibitors. While inhibition of neutrophil elastase is a function common to both alpha(1)-PI and SLPI, we showed previously that they exhibit different patterns of protection against antigen-induced changes in airway function in allergic sheep. Specifically, the protective effect seen with SLPI was similar to the profile of action of synthetic tryptase inhibitors in the model. Based on these data, and the fact that tryptase is a serine protease, we hypothesized that SLPI, but not alpha(1)-PI, would block tryptase-induced bronchoconstriction. To test this, we compared the responses to inhaled tryptase in five sheep without treatment or after treatment with either aerosol alpha(1)-PI (10 mg) or aerosol SLPI (50 mg). The doses of alpha(1)-PI and SLPI selected had been shown to be effective in previous antigen-provocation studies. Treatments were given 30 min before aerosol challenge with tryptase (500 ng). Tryptase alone increased (mean+/-SEM) pulmonary resistance (R(L)) 142 +/- 24% over baseline. Pretreatment with alpha(1)-PI had no effect on the tryptase response (R(L)increased 122 +/- 20%). Pretreatment with SLPI, however, blocked the tryptase-induced response (R(L) increased only 40 +/- 4% P<0.05 vs. tryptase). These are the first studies comparing the inhibitory activity of SLPI and alpha(1)-PI on inhaled tryptase-induced bronchoconstriction. We conclude that, in vivo, SLPI, but not alpha(1)-PI, can block tryptase-induced bronchoconstriction and that this activity may explain the differential effects of these two serine protease inhibitors on antigen-induced airway responses in allergic sheep.

Administration, Inhalation↗

PubMed1992

Influence of exercise-induced bronchoconstriction on refractoriness.

This study determined if the degree of exercise-induced refractoriness is determined by the degree of exercise-induced bronchoconstriction. In 12 patients with exercise-induced asthma (mean [SEM] age 27 [3] years) we performed 2 pairs of exercise challenges 45 min apart at different work loads on 2 days. Mean (SEM) total respiratory heat loss during low and high work loads was 3.4 (0.2) and 5.1 (0.4) kcal, respectively. After the first and second exercise challenge at low work loads, mean (SEM) SRaw increased by 107 (15) and 73 (16)% (n.s.), as compared to 361 (40) and 98 (25)% at high work loads (p less than 0.005). We found a correlation between the initial airways response and refractoriness (r = 0.58, p less than 0.005) and conclude that the degree of refractoriness after exercise-induced bronchoconstriction is in part dependent on the severity of exercise-induced bronchoconstriction.

Adult↗

PubMed1992

Vasoconstriction and bronchoconstriction induced by 2,5-di-(tert-butyl)1,4-benzohydroquinone, an endoplasmic reticular Ca2+-ATPase inhibitor, in isolated and perfused rat lung.

The microsomal Ca(2+)-ATPase inhibitor 2,5-di-(tert-butyl)-1,4-benzohydroquinone (tBuBHQ) induced bronchoconstriction and vasoconstriction in the isolated perfused and ventilated rat lung. These effects were accompanied by increased levels of thromboxane and prostacyclin in the effluent perfusate. The effect of tBuBHQ was inhibited by L-655,240, a thromboxane receptor antagonist, indicating thromboxane-A2-mediated bronchoconstriction and vasoconstriction. Accordingly, the cyclooxygenase inhibitor indomethacin largely blocked the effects of tBuBHQ. The involvement of a phospholipase in the generation of thromboxane A2(TXA2) was supported by dibucaine protection on tBuBHQ effects. The results from this study indicate that tBuBHQ, probably by inhibiting the microsomal Ca(2+)-ATPase, can trigger the arachidonic acid cascade leading to the formation of TXA2, which in turn causes bronchoconstriction and vasoconstriction in rat lung.

Animals↗