Increased consumption of polyunsaturated oils may be a cause of increased prevalence of childhood asthma.
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Biomedical subjects
Publications and source records attributed to C Salome.
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We compared the effects of pretreatment with saline, ipratropium bromide, and disodium cromoglycate (DSCG) on bronchoconstriction induced by methoxamine--an alpha-adrenoceptor agonist, in asthmatic subjects. All 12 patients bronchoconstricted in response to methoxamine after saline. The PD20 (the dose of methoxamine causing a 20% fall in forced expiratory volume in 1 s [FEV1]) ranged from 0.3-18 mumol. Ipratropium bromide (200 micrograms administered by aerosol) significantly inhibited (P less than 0.05) the response to methoxamine in all patients without producing significant changes in the mean baseline lung function. The mean PD20 for methoxamine after saline was 6.8 mumol and 95% confidence limits (CL) were 3.6, 12.7 mumol. The mean PD20 for methoxamine after ipratropium bromide was 35.4 (95% CL 28.8, 43.6) mumol. DSCG also produced significant (P less than 0.05) shifts to the right in the methoxamine dose response curves, but did not affect resting airway calibre as measured by the FEV1. The mean PD20 for methoxamine increased from 3.3 mumol (95% CL 1.1, 10.0 mumol) after saline to 25.1 mumol (95% CL 14.1, 44.6) after DSCG pretreatment. These findings suggest that alpha-adrenoceptors in the airways of asthmatic subjects may be located at sites other than smooth muscle--possibly on mast cells but more likely on nerve endings and/or parasympathetic ganglia.
The effect of 1 mg inhaled prazosin on bronchoconstriction induced by methoxamine was investigated in seven asthmatic subjects. Prazosin caused significant inhibition of the methoxamine-induced bronchoconstriction in six of the seven patients. These findings suggest that methoxamine produces bronchoconstriction in asthmatic subjects via stimulation of alpha-adrenoceptors. In previous studies propylene glycol has been used as a vehicle for delivery of prazosin. This substance was found to cause significant inhibition of methoxamine effects and to shift the dose response curve to histamine to the right in four of seven patients.
A rapid, simple method for measuring bronchial responsiveness to inhaled histamine is described. The method was used to obtain dose response curves in 50 atopic subjects with varying respiratory and nasal symptoms. The cumulative dose of histamine which caused a 20% fall in the one second forced expiratory volume (PD20-FEV1) varied between 0.046 and greater than 3.9 mumol and correlated with the severity of symptoms. The reproducibility of the PD20-FEV1, determined from duplicate measurements in 15 subjects with varying degrees of bronchial responsiveness was found to be satisfactory. When the PD20-FEV1 from this rapid method was compared with that obtained from the dosimeter method no significant difference was found. The dose delivered by this method was shown to be cumulative.
Tests of bronchial reactivity in man may help in understanding the nature of bronchial hyperreactivity which is characteristic of asthmatic subjects. Comparison of published studies is, at present, limited because diverse methods have been used to study and to report the results of bronchial provocation tests. The factors which affect the response include the type of provoking agent used, the method of delivery, the lung function test used, the method of expressing the result and "subject" factors. The effect of each of these factors is reviewed. Histamine and methacholine are the most useful substances for distinguishing normal from asthmatic subjects, the technique of provocation appears to have only a small effect on the results and, the FEV1 appear to be the best test for distinguishing asthmatic from normal subjects. It is recommended that, whenever possible, the whole dose response curve is reported with the percent change in FEV1 plotted against the dose delivered on a log scale.
In twelve subjects with perennial allergic rhinitis and stable asthma nasal obstruction was induced with histamine diphosphate solution introduced onto the nasal mucosa by a nasal atomizer in a cumulative manner starting with a 0.001% solution. The effect on the nose was measured by the change in inspiratory nasal flow resistance and the lung response was determined by the one second forced expiratory volume (FEV1). The test was stopped when there was a greater than 20% fall in FEV1 or when the total dose of histamine diphosphate reached 26 mumoles. All twelve subjects had a greater than six fold increase in inspiratory nasal flow resistance together with other symptoms of rhinitis in response to histamine. Six subjects had a dose related fall of greater than 20% in FEV1. Two others had falls of 10% and 17%. These changes persisted for between five and thirty minutes. In four subjects, aerosol salbutamol was needed for complete reversal of the FEV1. There was no relationship between the fall in FEV1 resulting from nasal stimulation and airway reactivity as measured by histamine inhalation test on a separate day. The results suggest that the airways of some asthmatics narrow in response to nasal stimulation.