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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bronchial hyperresponsiveness (BHR) is a major feature of asthma that is determined by both genetic and environmental factors. The assessment of BHR can be a valuable means of assessing asthma severity and also response to therapy. BHR can be measured with a variety of provocative agents including exercise, methacholine, histamine, hypotonic and hypertonic saline and cold air. Methacholine and histamine challenges have been well studied and standardized. They are extremely sensitive indicators of BHR, but this is not synonymous with asthma. This requires that the physician interprets the clinical significance of test results with caution.
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PMID:Bronchoprovocation in children. 179 15

Bronchial hyperresponsiveness is a constant feature of asthma even when airflow obstruction is absent. Detecting nonspecific bronchial hyperresponsiveness is useful when the diagnosis of asthma has not been confirmed or when a patient describes symptoms of cough, chest tightness, and dyspnea that cannot be ascribed to other causes. Also, because wheezing is a symptom of other disorders, inhalation challenge tests can be useful in defining its cause when reversible airflow obstruction has not been documented. A number of easy and safe techniques are available to detect nonspecific bronchial hyperresponsiveness. The histamine and methacholine challenge have had the most widespread use in the clinical pulmonary function laboratory. The exercise and cold air challenges are limited by expense. The osmotic challenge may gain more acceptance as experience with this technique grows. These different agents have the advantage of simplicity, reproducibility, a low number of adverse effects, and a high degree of specificity and sensitivity. A limited number of asthmatics show bronchial hyperresponsiveness to specific agents such as chemical sensitizers in the workplace, aeroallergens, aspirin, nonsteroidal anti-inflammatory agents, and sulfiting agents. Bronchoprovocation testing with these agents is usually reserved for the hospital laboratory because severe or delayed reactions may occur. These tests, however, can be extremely useful in defining a population of sensitive asthmatics.
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PMID:Bronchoprovocation testing. 266 Nov 16

Bronchial hyperresponsiveness (BHR) as the main condition for the development of asthma may be modulated either by intrinsic or by extrinsic stimuli as well as by climatic and meteorologic factors. Proinflammatory mediators in combination with alterations of airway mucosa induce or amplify BHR. Upper airway viral infections, exposure to allergens in atopic subjects, chronic hyperplastic changes of the upper airways, airway irritants and analgesics are supposed to be the most likely asthma triggers in predisposed children and adults. There is the suggestion that BHR can be improved not only by treatment with steroidal and nonsteroidal antiinflammatory drugs but also by maritime climatotherapy. The latter could be the result not only of the reduction of inhalative irritants, e.g. of allergen concentration, but also by the involvement or more complex mechanisms. Possible theoretic approaches and hypotheses regarding the mode of action of maritime climatic cures are discussed. First preliminary results obtained in a mediterranean region have demonstrated a negative impact of metereologic events like passages of cold weather fronts or increase of wind velocity on the course of asthma disease. An improvement of BHR assessed by histamine challenge test has been observed at the end of climatotherapy in the Baltic sea area. Prospective studies about asthma prevention in subjects at risk with BHR and atopy that have been starting should contribute to the evaluation of the therapeutic effects and the prognostic importance of maritime climatotherapy for getting exact scientific indications for climatotherapy in patients with bronchial asthma.
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PMID:[The effect of climatic and meteorologic factors on bronchial hyperreactivity and the course of bronchial asthma diseases and their potential significance in asthma prevention: hypotheses, methodologic approaches and initial results]. 268 20

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.
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PMID:[Bronchial hyperreactivity]. 379 4

The Ca2+ requirements for excitation-contraction coupling in smooth muscle may be satisfied from both intracellular and extracellular sources, the relative extent of use of which is both tissue- and stimulant-dependent. Extracellular Ca2+ is apparently mobilized through two separate pathways, receptor operated (ROC) and potential dependent (PDC) Ca2+ channels. The latter process is sensitive to the Ca2+-channel antagonists, a heterogeneous group of compounds including verapamil, nifedipine and diltiazem. Ca2+ mobilization in respiratory smooth muscle is reviewed. The available evidence for this multiple stimulant-sensitive system indicates that both intra- and extracellular sources of Ca2+ are used. Data from bovine, canine and guinea pig tracheal muscle indicate, from studies of Ca2+-dependence of response and Ca2+ channel antagonist sensitivity, that the extent of use of extracellular Ca2+ lies in the order K+ greater than histamine greater than or equal to 5-hydroxytryptamine greater than acetylcholine. The bronchodilator activity of the Ca2+ channel antagonists is noted. Bronchial hyperreactivity is characterized by an increased sensitivity to a variety of stimulants including cold air, exercise, histamine and acetylcholine. The possible origins of this defect are noted. It is suggested that a defect in Ca2+ mobilization or in the receptor - Ca2+ mobilization coupling process at the level of the smooth muscle may constitute an important underlying cause of bronchial hyperreactivity. Potential analogies to reactivity changes seen in hypertensive vascular smooth muscle are noted.
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PMID:Calcium, the control of smooth muscle function and bronchial hyperreactivity. 630 6

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.
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PMID:Mediators and non-specific bronchial hyperreactivity. 636 Jul 2

Bronchial hyperresponsiveness (BHR) describes the exaggerated bronchoconstrictor response to a host of stimuli such as cold air or exercise that occurs in most patients with asthma. It is an important feature of asthma because BHR correlates with diurnal peak expiratory flow variation, bronchospasm following exercise, the need for asthma medications, and asthma severity. Many studies published in the past year have increased our understanding of BHR. First, epidemiologic studies have revealed BHR to be a risk factor for the subsequent development of asthma. BHR is also more common in children than adults, and the persistence of BHR is related to atopy. Second, genetic and pathophysiologic studies have improved our understanding of the etiology of BHR. The genetic basis for BHR, atopy, and asthma was further elucidated with the finding of a cluster of potential candidate genes for asthma susceptibility on chromosome 5. In addition, eosinophilic infiltration and basement membrane thickening of the airways, both characteristic findings noted in patients with asthma, were found to correlate with pulmonary function and degree of BHR. Lastly, studies on treatment of BHR confirmed the beneficial effects of inhaled glucocorticoid therapy and allergen avoidance on BHR in children with asthma. In addition, a new type of asthma medication, the leukotriene inhibitors, has been shown to decrease BHR in adults with asthma and may eventually prove to be an effective medication for children with chronic asthma.
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PMID:The etiology and control of bronchial hyperresponsiveness in children. 901 42

There is little information of lower respiratory symptoms, bronchial hyperresponsiveness and airway inflammation in elite ice hockey players. A total of 88 highly trained ice hockey players and 47 control subjects were studied. All the subjects were subjected to skin-prick tests, resting spirometry examinations and histamine-challenge tests. Adequate induced sputum samples were obtained from 68 of the ice hockey players and from 18 symptom-free control subjects on a separate day. Bronchial hyperresponsiveness in a histamine-challenge test was found in 21 (24%) of the athletes and in five (11%) of the controls. Current asthma (current asthmatic symptoms and increased bronchial responsiveness) was observed in 13 (15%) of the athletes and in one (2%) of the control subjects. Total asthma (current asthma or previously physician-diagnosed asthma) occurred in 19 (22%) of the athletes and in two (4%) of the controls. Atopy, according to skin-prick tests, was observed in 51 (58%) of the athletes and 17 (36%) of the control subjects. The differential cell counts of eosinophils (2.6 versus 0.2%) and neutrophils (80.9 versus 29.9%) in the sputum samples of the ice hockey players were significantly higher than in those of the control subjects. Asthma is common in elite ice hockey players and they show signs of a mixed type of neutrophilic and eosinophilic airway inflammation. Inhalation of cold air associated with exposure to indoor pollutants during intensive training is a possible causative factor.
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PMID:Airway inflammation, bronchial hyperresponsiveness and asthma in elite ice hockey players. 1288 60

Important asthma outcomes such as lung function and bronchial hyperresponsiveness are probably determined in early childhood. Early and longitudinal objective assessment of lung function and bronchial hyperresponsiveness is necessary to enable early diagnosis, monitor intervention and improve prognosis in preschool children. Cold air challenge and plethysmographic measurement of specific airway resistance (sRaw) are feasible candidate methods for diagnosis, clinical monitoring and research during this critical period of lung growth and development. Methodology and practical aspects of cold air challenge and assessment of sRaw in preschool children are reviewed. Reference values are provided for sRaw and have allowed discrimination between health and respiratory disease, both in cross-sectional and longitudinal studies. Bronchial hyperresponsiveness can be determined with acceptable repeatability and provides good discrimination between asthmatics and healthy. The effects of classic anti-asthmatic therapies have also been documented with these techniques. The need for further standardisation and improvement of these methods and future perspectives are outlined.
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PMID:Cold air challenge and specific airway resistance in preschool children. 1629 8