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At least 19 recordsLinked to original sources
PubMed1980

A comparison between different methods for detecting bronchial hyperreactivity. Bronchial hyperreactivity: methods of study.

The authors evaluated bronchial hyperreactivity comparing two different methods for aspecific bronchostimulation (H2O ultrasonic mist and free running) and a bronchodilation test. The investigation had been carried out on three groups of subjects. The first included 15 nonsmoking normal subjects, the second 23 asthmatic patients and the third 16 rhinitic patients. All subjects were submitted to bronchodynamic tests in three different ways. The ventilatory parameters were FVC, FEV1, MMEF and Vmax25. In normal subjects no significant changes were found. In asthmatic patients the bronchodilation test was positive in 65% of the cases, regarding FEV1 and in 87% regarding the forced flows. The running test was positive in 26% of the cases (FEV1) and in 61% of the cases (forced flows). The ultrasonic mist caused a significant drop in FEV1 in 17% of the cases, while flows were significantly reduced in 30% of the cases. In rhinitic patients the bronchodilation test was positive in 25% of the cases both considering FEV1 and forced expiratory flows. Ultrasonic mist never induced a decrease of FEV1, while flows decreased in 12.5% of the cases. The free running test was positive in 12% of the cases regarding FEV1 and in 25% regarding forced flows.

Adolescent↗
PubMed1994

[Mechanisms of bronchial hyperreactivity. Bronchial edema, mechanical and vascular factors].

Hindrance to gas flow in the bronchi is affected not only by airway smooth muscle tone but also by airway circulation. Congestion and oedema increase airway wall thickness and act in series with airway smooth muscle contraction to reduce airway calibre, an effect which is more marked in small and intermediate bronchi. Many mediators, neuromediators, paracrine mediators produced by resident (epithelium) or migrant (inflammatory cells) cells share bronchomotor and vascular effects. In addition, contraction of airway smooth muscle and vascular phenomena are mechanically coupled. Contraction of airway smooth muscle facilitates vascular congestion and oedema because the diameter of the muscle ring is more reduced than the external diameter of the airways. In addition, a negative intrathoracic pressure, e.g. in asthma, increases the mechanical loading of both ventricles, thereby facilitating pulmonary and bronchial oedema. The effects of this mechanical coupling are enhanced by airway inflammation that facilitates both vascular congestion and leakage. Stimuli such as exercise and hyperventilation cause airway vasodilatation which, in turn, facilitates and, possibly, triggers the post-exercise asthma attack. Conversely, congestion and vasodilatation may have a protective effect through an increase in the clearance of bronchoconstrictor substances, or in reducing the amplitude of airway cooling and water loss in exercise-induced asthma. The relative role in bronchial hyperresponsiveness of airway smooth muscle contraction and vascular phenomena probably depends upon individual factors such as, for instance, both intensity and nature of inflammation of the airway walls.

Airway Obstruction↗
PubMed1980

Experimental induced bronchial hyperreactivity.

Bronchial hyperreactivity can be influenced by antigen inhalation as well as by infections which affect the bronchial tree. Bronchial hyperreactivity characterizes the obstructive airway diseases. In order to study this problem, we have performed in our laboratory a series of experiments concerning this problem. The influence of proteolytical enzymes on acetylcholine-induced bronchoconstriction was tested in a series of animals. After enzymes inhalation, an extreme enlarged answer to acetylcholine exposure was observed. Bronchial hyperreactivity induced after histamine and also after antigen administration and the influence of antihistamine was also tested in a series of experiments. The hyperreactivity of bronchial system observed after experimental pulmonary embolism was finally studied on a series of animals. The influence of vagus blockade on this induced bronchial hyperreactivity was also tested. After vagus blockade no bronchoconstrictoric answer was observed. The relation of bronchial hyperreactivity to localization of sensoric receptors can be assumed.

Acetylcholine↗
PubMed1991

[The functional diagnosis of bronchial hyperreactivity and bronchial lability in children with bronchial asthma].

During a remission, bronchial asthma children were examined for bronchial hyperreactivity and bronchial lability by means of graded physical exercise tests, and pharmacological tests with bronchoconstrictors and bronchodilators. It has been established that normal lung function seen during aa remission does not mean the lack of bronchial hyperreactivity whereas incomplete recovery of bronchial patency during bronchial asthma remission is always attended by bronchial hyperreactivity in almost all the cases. In carrying out functional tests for bronchial hyperreactivity and bronchial lability, the recording of the velocity parameters of forced expiration making it possible to define patency of not only the central but also of the peripheral bronchi appeared very informative.

Asthma↗
PubMedDate not supplied

[Bronchial hyperreactivity].

Bronchial hyperreactivity is a condition in which the airways show a much greater bronchoconstriction response to provocative stimuli than what is normal. The stimuli may be specific (different allergens) or non-specific (exercise, infection, cold, air, ozone, kerosene or a variety of inhalant irritants). The normal control of the airways is regulated by: parasympathetic cholinergic nerves, sympathetic adrenergic nerves and non-adrenergic bronchodilator system. The activity in all these pathways regulates bronchomotor tone which is affected by many different reflexes. Such changes play a role in hyperreactivity. Exposure to allergens is another cause of inflammation and specific hyperreactivity which may increase the degree of non-specific bronchial reactivity. Inheritance has been implicated in bronchial hyperreactivity according to animal experiments and human twins studies. Calcium ions are involved in most cellular processes and their role in bronchial hyperreactivity is related to defects in calcium regulation and metabolism. Based on this speculation, calcium antagonist drugs have been used in the treatment of bronchial asthma, though no clinical improvement has been observed by most authors.

Asthma↗
PubMed1988

Fate of grainhandlers with bronchial hyperreactivity.

Bronchial reactivity to methacholine and to grain dust were determined in a group of grainhandlers whose spirometry was being studied prospectively. Six workers showed specific bronchial responses to grain dust (indicative of occupational asthma), 21 did not show reactivity to grain dust but had bronchial hyperreactivity to methacholine and 40 had neither. Those with hyperreactivity were older, had lower FEV1 at initial examination and were more likely to experience a significant decline in FEV1 over a single working shift. Over 6 years of follow-up, those with hyperreactivity were not more likely to leave work and although they showed a more rapid decline in lung function over the period, because of the small number of individuals studied the difference between those with and without bronchial hyperreactivity was not significant. Among those with hyperreactivity to methacholine, there was a significant positive association between change in FEV1 over a single workshift and change in FEV1 over six years of followup, not seen in those without hyperreactivity to methacholine. Moreover, reactivity to methacholine was a stable observation over 6 years in the majority of studied individuals. We conclude that in the presence of bronchial hyperreactivity to methacholine, change in FEV1 over a single workshift more precisely predicts the trend in FEV1 over time in grainhandlers.

Adult↗
PubMed1991

[Bronchial hyperreactivity].

Bronchial hyperreactivity, the abnormal reaction of the airways on non-allergic stimuli, is a feature of patients with chronic nonspecific lung disease. Several underlying mechanisms such as the neurogenic pathways, inflammatory cells and mediators, increased vascular leakage, epithelial damage and pathological changes in airway smooth muscle seem to play a role of importance in bronchial hyperreactivity. Recent developments in these research fields produce more clarity in the mutual connection of these factors in relation to the phenomenon of bronchial hyperreactivity.

Adrenergic Fibers↗
PubMed1989

[Bronchial asthma and bronchial hyperreactivity].

Bronchial hyperreactivity to allergens and non-allergic stimuli is a feature of most patients with asthma as measured by the response to inhalants as pharmacological agents and physical stimuli. In contrast to adults there is an obvious relation of asthmatic episodes to allergen exposure in childhood. However, the development and persistence of bronchial hyperreactivity is well described by interaction of inflammation cells and their mediators. Not only the severity of asthma is related to the severity of bronchial hyperresponsiveness but also the therapeutic strategies.

Asthma↗
PubMed1975

Bronchial hyperreactivity.

Bronchial hyperreactivity is characterized by increased responsiveness of bronchial smooth muscle to non-specific constrictor stimuli. Tests used in assessing airway calibre are influenced by a number of factors and should be regarded as providing a qualitative rather than quantitative index of reactivity. One important determinant of bronchial reactivity is the resting state of the airways. An increase in resting bronchomotor tone either by the direct action of spasmogens or by the autonomic nervous system may potentiate a subsequent constrictor stimulus. Bronchial challenge may help in the diagnosis of asthma in patients with normal lung function at the time of testing.

Airway Obstruction↗
PubMed1983

Mediators and non-specific bronchial hyperreactivity.

Bronchial hyperreactivity is a major if not an essential characteristic of bronchial asthma. The relation between mediators and non-specific bronchial reactivity is an essential question in the pathogenesis of bronchial asthma. This is reflected in the different hypotheses on pathogenesis. The bronchial reaction to mediators is determined by the pre-existing degree of non specific bronchial reactivity. Bronchial reactivity to histamine or prostaglandin F2 alfa is related to the bronchial metacholine-reactivity. The bronchial lability to exercise or cold air and the immediate bronchoconstriction after allergen inhalation are also determined by the non specific bronchial reactivity. On the other hand, several observations support the concept that mediators modify the non specific bronchial reactivity. The non specific bronchial reactivity increases during the pollen season. Disodiumcromoglycate, a known inhibitor of mediator release, prevents the seasonal increase in bronchial reactivity. The increased bronchial reactivity in patients with allergic rhinitis may also be related to local mediator release. Exposure to ozone and viral upper respiratory tract infections enhance the bronchial reactivity. Avoidance of house dust mite exposure in mite sensitive asthmatics decreases the bronchial reactivity. The same observation has been made after withdrawal from occupational exposure. In experimentally induced asthma, the late asthmatic reaction after allergen inhalation is followed by an increase in nonspecific bronchial reactivity. Mediator release may enhance non specific bronchial reactivity in several ways. Increase of mucosal permeability, modification of sensory nerve endings, alteration of the efferent vagal motor pathway, enhancement of the effect of other mediators, influx of secondary cells, modification of cell receptors and changes in smooth muscle contractility have all been suggested. Mediator release and non specific bronchial reactivity thus appear to be interrelated characteristics of bronchial asthma. Individual differences in the clinical importance of the two characteristics may have therapeutic significance.

Allergens↗
PubMed1980

Clinical implications of bronchial hyperreactivity.

Bronchial hyperreactivity may be a primary internal factor needed for the occurrence of asthmatic symptoms when the atopic individual meets with allergens or the non-atopic individual inhales irritants causing inflammatory reactions in the bronchial tree. It can also be a secondary expression of allergy and occupational exposures. The hyperreactivity can be affected by treatment and is therefore a valuable tool to judge experimental studies of background and predictive factors, for follow up of specified airways disease and for treatment and drug effects. It is necessary to collect sufficient background factors and to use proper dose-response studies. We still lack knowledge as to why presumed normal subjects react, is it due to undetected small airways disease? Do we need to measure both sensitivity (as threshold values) and reactivity (as dose response-curves) in all kinds of tests of bronchial reactivity? We need simple ways to test larger populations in prospective studies of workers exposed to occupational irritants in order to solve the problems of primary versus secondary, acquired hyperreactivity.

Allergens↗
PubMed1985

Influence of drug therapy on bronchial hyperreactivity.

Bronchial hyperreactivity was confirmed in eleven nonselected patients with chronic respiratory disease during a period of quiescence by inhalative provocation with histamine. After one week's treatment with ketotifen a protective effect against the histamine-induced bronchospasm was observed in nine patients. The rapid appearance of this protective mechanism was demonstrated both in patients with exogenous and endogenous bronchial asthma and in the three patients with chronic bronchitis. Regardless of the fact that specific bronchospasmolysis is the main therapeutic measure, based on our experience the protective mechanism of mast-cell stabilizers as supplementary therapy is at present at an earlier point of time than is generally assumed.

Adult↗
PubMed1994

[Comparative study of 2 diagnostic tests of aspecific bronchial hyperreactivity].

Bronchial challenge test are useful in diagnosis of bronchial hyperresponsiveness (BH). To assess the sensitivity of histamine test (HT) and exercise test (ET), 45 asthmatic patients (31 men, 14 women, ages 9-34) with normal resting pulmonary function test were studied. HT and ET were performed in two different days. HT was positive in 40 (6 severe, 23 moderate and 11 mild) and ET was positive in 13 (88.8% vr 28.8%, p < 0.001). All patients with positive ET had positive HT. There is a relationship between the degree of BH severity and the response to ET (chi 2 = 5.995; p < 0.05). The HT has a high profitability the diagnosis of BH. The ET has a low sensitivity.

Adolescent↗
PubMed1986

Bronchial hyperreactivity and bronchial obstruction in respiratory viral infection. An attempt to evaluate the relationship.

The aim of this study was to investigate the relation of viral respiratory infection with bronchial hyperreactivity and bronchial obstruction. A viral infection using a live attenuated influenza virus was induced successfully in 10 of 30 patients with chronic obstructive pulmonary disease (COPD) and in 3 subjects without COPD (non-COPD). No significant change in bronchial reactivity and lung function could be found in comparison with the baseline values.

Administration, Intranasal↗
PubMed1994

[Asthma and nonspecific bronchial hyperreactivity].

Bronchial hyperresponsiveness is a hallmark of asthma although it can also be present, to a lesser extent, in other diseases. The level of bronchial responsiveness depends on immuno-inflammatory processes modifying the functional status of airway smooth muscle as well as the structure of the bronchial wall. The responsiveness toward a direct constricting pharmacological agent is poorly correlated to the one toward an indirect constricting agent or a physical stimulus which cause airway obstruction through a more complex mechanism. Transversal studies show a relationship between the severity of asthma and the level of methacholine airway responsiveness. Long term treatment with corticoids can reduce the bronchial hyperresponsiveness of asthmatics.

Airway Obstruction↗
PubMed1993

Intratracheal E. coli lipopolysaccharide induces platelet-dependent bronchial hyperreactivity.

Bronchial hyperresponsiveness (BHR) characterizes asthma and accompanies respiratory infections. Because endotoxin [lipopolysaccharide (LPS)] induces either hyper- or hyporesponsiveness of the guinea pig airways and protects against bronchopulmonary anaphylaxis in sensitized guinea pigs, we compared the effects of the intratracheal administration of Escherichia coli LPS on bronchopulmonary responsiveness to intravenous serotonin or acetylcholine in sensitized and nonsensitized guinea pigs. LPS (1 mg) induced BHR within 1-2 h, with a threefold increase in the bronchial response after serotonin challenge in both groups (n = 6; P < 0.005) and a marked influx of neutrophils into the perivascular and peribronchial connective tissue and the bronchoalveolar lavage fluid. This BHR was not leukocyte dependent, since it was still observed in animals depleted of circulating leukocytes with vinblastine and was not modified by antineutrophil serum, unless platelet counts were < 100,000/mm3. This suggested that LPS-induced BHR involves platelets, and indeed antiplatelet serum, which depleted platelets, or prostacyclin, which inhibited platelets, was effective in suppressing BHR. Neither aspirin, mepyramine, nor the platelet-activating factor antagonist WEB 2170, administered before LPS instillation, prevented BHR, whereas the association of methysergide, mepyramine, and aspirin was effective, without modifying platelet and leukocyte counts. This association has been shown to prevent the release of ATP by ex vivo platelets. Our results suggest that platelets or a platelet-derived product mediates LPS-induced BHR.

Acetylcholine↗
PubMed1993

[The effect of ultraviolet-irradiated blood on bronchial hyperreactivity in bronchial asthma patients].

Clinical investigation was carried out with the view to study the effect of ultraviolet-irradiated autoblood on bronchial spasm induced by acetylcholine in 11 patients with moderate and severe bronchial asthma in out-of-attack period. Reinfusion of autoblood was established to reduce bronchial hyperresponsiveness in asthma thus allowing to control one of the main pathogenetical mechanisms.

Acetylcholine↗
PubMed1984

Upper airway disease and bronchial hyperreactivity.

Bronchial irritability is seen in illnesses involving the upper respiratory tract. In allergic rhinitis, it appears to coexist, and constitutes a risk factor for the development of asthma. In acute respiratory infections, asthmatic attacks may occur coincidentally with viral infections, and infection with some viruses may cause normal persons to develop bronchial irritability. There is suggestive evidence that the associated bronchial irritability may take months to clear and may predispose subjects to permanent hyperreactivity.

Asthma↗