Bronchoconstriction

Abstract: Inhalation of histamine diphosphate aerosol (16 per cent, 10 breaths) produced a 218 ± 546 per cent (mean ± SE) increase in airway resistance in 16 normal subjects with colds compared with a 305 ± 55 per cent increase in 11 healthy control subjects (P < 001) There was no significant difference in mean baseline airway resistance between the two groups Inhalation of saline produced no significant change in airway resistance in either group Isoproterenol hydrochloride (05 per cent, 1 breath) or atropine sulfate aerosol (02 per cent, 20 breaths) each reversed and prevented the increase in airway resistance by histamine, indicating that the bronchoconstriction was caused by smooth muscle contraction and that post-ganglionic, cholinergic pathways were involved in the mechanism In 6 subjects with colds, citric acid aerosol (10 per cent, 5 breaths) caused bronchoconstriction that lasted up to 30 sec after inhalation, a significantly greater effect than that observed in control subjects or in the same s

Abstract: Quantitative measurement of nonspecific bronchial responsiveness can be simply and reproducibly made by inhalation tests with histamine or methacholine. Responsiveness to histamine correlates closely with responsiveness to methacholine. The degree of responsiveness relates closely with the presence and severity of asthma. The greater the increase in responsiveness the lower the peak flow rate (PFR) on waking, the greater the improvement in PRF after bronchodilator, the greater the diurnal variation of PFR, the easier is bronchoconstriction induced by nonspecific and allergic stimuli and the more treatment is required to control symptoms. Nonspecific responsiveness can be increased by exposure to respirable allergens or occupational sensitizers, and by infection. The observations suggest that measurement can be used in clinical practice to diagnose the presence of asthma, to help assess the severity of asthma and, in the assessment of occupational asthma, to determine if exposure can heighten bronchial responsiveness.

Abstract: Six patients with chronic cough, without history of dyspnea or wheezing, had normal base-line spirometry but hyper-reactive airways, as demonstrated with methacholine. Maintenance therapy with bronchodilators promptly eliminated the cough in all patients. Three to 12 months later therapy was discontinued for three days, cough returned, and detailed pulmonary-function studies were carried out. Again, base-line values were normal, but after methacholine one-second forced expiratory volume decreased an average of 40 per cent in the patients as compared to 30 per cent in normal controls (P less than 0.001). The point of identical flow was increased by methacholine to 43.5 per cent of vital capacity in the patients, as compared to 6 per cent in normal controls (P less than 0.001), and the alveolar plateau was 4.8 deltaN2 per liter, as compared to 1.4 in normal controls (P less than 0.01). Specific airway conductance was lowered in patients and controls, but the post-methacholine value was significantly lower in the patients. On the basis of their persistently hyper-reactive airways, inducible diffuse airway bronchoconstriction and excellent response to bronchodilator therapy, these patients appear to have a variant form of asthma in which the only presenting symptom is cough.

Abstract: This relates to methods and devices for treating reversible chronic obstructive pulmonary disease, and more particularly, relates to a device for exchanging energy with airway tissue such as that found in the airway of human lungs. The exchange of energy with this airway tissue in the airways reduces the ability of the air ways to constrict and/or reduces the resistance within the airway to the flow of air through the airway. This also relates to a method for decreasing responsiveness or decreasing resistance to airflow of airways involves the transfer of energy to or from the airway walls to prevent or reduce airway constriction and other symptoms of lung diseases. The treatment reduces the ability of the airway to contract during an acute narrowing of the airways, reduces mucus plugging of the airways, and/or increases the airway diameter. The methods according to the present invention provide a longer duration and/or more effective treatment for lung diseases than currently used drug treatments, and obviate patient compliance issues. This also includes additional steps that reduce the ability of the lung to produce at least one of the symptoms of reversible obstructive pulmonary disease and to reduce the resistance to the flow of air through a lung.