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At least 865 records · Page 48Linked to original sources
PubMed1990

The effect of 2 weeks treatment with cetirizine on bronchial reactivity to methacholine in asthma.

1. We investigated the effect of 2 weeks therapy with oral cetirizine (10 mg twice daily) on methacholine bronchial reactivity in 14 asthmatics. All had bronchial hyperreactivity to methacholine on entry to the study, with a geometric mean cumulative PC20 of 0.83 mg ml-1 (range 0.1-3.61 mg ml-1) and eight were atopic on skin prick testing. 2. The study was placebo-controlled and in randomised order, with a minimum 1 month washout period between cetirizine and placebo study periods. Four methacholine challenges were performed in all, at the beginning and at the end of each study period. 3. No significant change in methacholine reactivity was found following 2 weeks therapy with cetrizine. The repeatability coefficient for the PC20 methacholine over 2 weeks was found to be 2.90 doubling dilutions for the placebo period and 1.73 doubling dilutions for the cetirizine period. The study had a 80% power at the 5% significance level (two-tailed) to detect a 1.16-doubling concentration change in methacholine reactivity. 4. We conclude that 2 weeks therapy with cetirizine has no significant effect on non-specific bronchial hyperreactivity.

Adult↗
PubMed1990

Effect of formoterol, a long-lasting beta 2-adrenoceptor agonist, against methacholine-induced bronchoconstriction.

1. The effects of a new long-acting inhaled beta 2-adrenoceptor agonist aerosol formoterol (12 micrograms), on FEV1, and on methacholine-induced bronchoconstriction, were compared with those of terbutaline (250 micrograms) and placebo in 12 midly asthmatic subjects. 2. PC20, the concentration of methacholine needed to cause a 20% fall in baseline FEV1, was determined 2 and 5 h after formoterol, terbutaline and placebo on separate days. Baseline PC20 was determined on a different day. 3. Compared with terbutaline and placebo, formoterol hastened recovery from methacholine-induced bronchoconstriction, and significantly increased mean PC20 (by 2.2- and 2.9-fold at 2 and 5 h respectively). 4. Thus, formoterol has a protective effect against methacholine-induced bronchoconstriction which lasts for at least 5 h.

Adrenergic beta-Agonists↗
PubMed1990

Comparative effects of dilevalol and atenolol on lung function and airway response to methacholine in hypertensive subjects.

1. In this double-blind randomized study, after a 4-weeks placebo period, 18 patients with mild to moderate primary hypertension were assigned to treatment with either dilevalol (n = 9) daily or atenolol (n = 9) over a period of 3 months. 2. Expiratory flows, lung volumes and airway responsiveness (AR) to methacholine were assessed at the end of the placebo period and after an active treatment of 12 weeks. Blood pressure (BP), heart rate (HR) and ECG were monitored during the methacholine challenges. Twice daily peak expiratory flow rates and respiratory symptoms were recorded on a diary card. 3. No significant effects on ECG, HR and BP were observed after methacholine inhalation. In all but one subjects there was no significant change in expiratory flows, lung volumes or AR throughout the study. Mean FEV1, FVC, PEFR, FRC and PC20 methacholine were unchanged after 3 months of treatment, and not statistically different between patients on dilevalol or atenolol. 4. One subject, without previous history of asthma, developed transient airflow obstruction 8 weeks after beginning dilevalol. 5. Dilevalol and atenolol have no significant effects on pulmonary function and AR in most subjects with no baseline airflow limitation. 6. Airflow obstruction may develop in normal subjects on dilevalol. Methacholine challenges are safe in subjects with uncomplicated hypertension.

Adult↗
PubMed1978

Tests to establish the diagnosis in cholinergic urticaria.

Methods for establishing the diagnosis in cholinergic urticaria are reviewed and compared. Provocation by exercise or hot bath is more effective than local provocation by intradermal tests. Of the intradermal tests, responses to nicotine acid tartrate and acetyl beta methylcholine chloride are positive only in patients with the more severe, readily induced eruptions. Furthermore, intradermal testing is not always reproducible in the same patient. In our patients, exercise proved the simplest, most effective diagnostic test.

Adolescent↗
PubMed1984

Sweat production in the isolated eccrine sweat gland of the rat.

A method has been developed to isolate a single rat eccrine sweat gland, together with the attached sweat duct, and to induce sweat secretion directly from the gland in vitro. Sweat production was induced using carbachol (2 X 10(-5) M to 3 X 10(-5) M) and methacholine (2 X 10(-5) M) in isolated plantar sweat glands maintained in a suitable environment (modified Krebs-Ringer bicarbonate at 38 degrees C containing 30% w/v fresh rat serum). The output of sweat was measured every 5 minutes for 85 minutes and the maximal final volume obtained with any one gland was 23 nl. Sweat production ceased on administration of appropriate concentrations of atropine (1 X 10(-5) M to 5 X 10(-5) M), withdrawal of calcium ions from the bathing fluid, and reduction of the medium temperature to 4 degrees C.

Animals↗
PubMed1986

Electrical field stimulation of isolated primate sweat glands.

An in vitro method is described for inducing secretion in isolated monkey eccrine sweat glands by means of electrical field stimulation (EFS). Ultrastructural analyses of these glands revealed unmyelinated nerve fibres surrounding the secretory coils. Numerous small clear vesicles, characteristic of cholinergic nerve terminals, were observed, along with a few which were large and dense-cored. EFS elicited an immediate secretory response which ceased abruptly upon termination of the current. The response was inhibited in a dose-dependent manner by atropine (IC50 1.5 X 10(-9) mol/l). Although most glands were completely inhibited by atropine, a minor atropine insensitive component was operative in some preparations. Physostigmine (10(-6) mol/l) potentiated the response to subthreshold EFS. Lidocaine (3 X 10(-4) mol/l) completely and reversibly blocked EFS but had no effect on methacholine (10(-6) mol/l) induced secretion. These results confirm that eccrine sweat gland activation is predominantly via cholinergic pathways and that EFS of isolated glands may be a useful model to study the control of secretory function in normal and diseased states.

Animals↗
PubMed1976

Factors in allergen-induced asthma: relevance of the intensity of the airways allergic reaction and non-specific bronchial reactivity.

Early asthmatic responses (EAR) of similar severity were produced by allergen inhalation challenges in nine asthmatic subjects. The severity of the airways allergic reaction was estimated by measuring the skin test weal size produced by the same dilution of allergen which caused the EAR. The non-specific bronchial reactivity was assessed by inhalation of incresing concentrations of histamine acid phosphate. Possible relationships between the severtiy of the airways allergic reaction, the level of non-specific bronchial hyper-reactivity and the pattern of asthmatic response were examined. There was a marked inverse correlation between the required severity of the airways allergic reaction and the non-specific bronchial reactivity (log10) of the individual (r = -0-96, P less than 0-001). The EAR was followed by a late asthmatic response (LAR) in five subjects. There was no evident correlation between the magnitude of the EAR and that of the LAR. In addition, no correlation was obtained between the pattern of response interms of EAR or LAR and the severity of the allergic reaction, or the level of non-specific bronchial reactivity. These results indicate that the allergic reaction and the non-specific bronchial reactivity are interrelated in the production of allergen-induced asthma. Thus a mild allergic reaction will induce and EAR in patients with markedly increased non-specific bronchial reactivity, whereas a severe allergic reaction is required to produce an EAR in those with only slightly increased non-specific reactivity. The lack of correlation between the occurrence of the LAR and the intensity of the airways allergic reaction, the non-specific bronchial reactivity and the intensity of the EAR indicates that other factors are involved in the development of LAR.

Adolescent↗
PubMed1977

Allergen-induced increase in non-allergic bronchial reactivity.

Non-allergic bronchial hyper-reactivity is a feature of most patients with asthma. We have measured non-allergic bronchial reactivity to inhaled histamine and methacholine in thirteen asthmatic subjects before and after allergen inhalation in the laboratory. The allergen inhalation produced mild early asthmatic responses (19-40% FEV1 fall) in all thirteen, additional definite late asthmatic responses (17-29% FEV1 fall) in four, and equivocal late asthmatic responses (5-11% FEV1 fall) in five. Following allergen inhalation, non-allergic bronchial reactivity increased in seven for up to 7 days. The seven included all four with definite late asthmatic responses and three of the five with equivocal late asthmatic responses. We conclude that allergens make asthma worse, partly through non-allergic mechanisms, and that avoidance of allergens is important in reducing non-allergic bronchial hyper-reactivity.

Allergens↗
PubMed1978

Atopy and bronchial reactivity in Australian and Melanesian populations.

In order to compare the prevalence of atopy and bronchial hyperreactivity among Papua New Guinian (P.N.G.) and Australian populations, skin prick tests and methacholine bronchial challenge tests were performed. A civilian and an army population from each country were examined and those with past or present asthma, recent respiratory tract infection and chronic lung disease were excluded. No statistical difference in the prevalence of atopy was found between the four populations. In the P.N.G. population 40 and 49%, and in the Australian population 27 and 39%, were found to be atopic, without symptoms of past or present allergic disease. The house dust mites were the commonest allergens in all populations. In response to methacholine (0.3 mg), only 6% of subjects had falls in 1 sec forced expiratory volume (FEV1) of more than 12% (upper limit of normal range) and only two were in the asthmatic range. There was no correlation between the degree of bronchial hyperreactivity and atopic status; however, the degree of bronchial hyperreactivity was slightly greater in the New Guinea civilian than in the Australian civilian population. In the absence of asthma, atopic status does not appear to cause increased bronchial reactivity, suggesting that some factor other than atopy must be present for the development of bronchial hyperreactivity characteristic of asthma.

Adolescent↗
PubMed1978

Effect of Sch1000 in allergen-induced asthma.

Carefully controlled allergen inhalation tests were carried out in twelve subjects to provoke early asthmatic responses with a mean maximum FEV1 fall of 30.7 +/- 5.2% (mean +/- s.d.). Four subjects had additional late asthmatic responses with a maximum mean FEV1 fall of 21.0 +/- 5.9%. The tests were repeated at intervals of 7 days in an identical way, following inhalation of Sch1000 (80 microgram) and placebo, each given 45 min before the onset of the early asthmatic response. This dose of Sch1000 produced a marked and uniform inhibition of methacholine-induced bronchoconstriction in the same subjects. The allergen-induced responses were reproducible in eleven out of the twelve subjects; the coefficient of variation for the decrease in FEV1 in the early responses being +/- 7% and in the late response +/- 43%. Sch1000 produced a slight and variable inhibition of early asthmatic responses (P less than 0.02) and no inhibition of late asthmatic responses. We examined the relationship between the degree of inhibition of the early asthmatic response by Sch1000 and : (a) the degree of inhibition produced by Sch1000 on histamine- and methacholine-induced bronchoconstriction; (b) the level of non-specific bronchial reactivity measured by inhaled histamine and methacholine; and (c) the degree of bronchodilatation produced by Sch1000. No relationship was found.

Administration, Intranasal↗
PubMed1979

A controlled study on the preventive effect of ketotifen, an antiallergic agent, on methacholine-induced bronchoconstriction in asthmatics.

We studied the preventive effect of ketotifen, an oral drug with antianaphylactic and antihistaminic properties on methacholine-induced bronchoconstriction in controlled cross-over experiments in twenty-six adult patients with extrinsic asthma. Both a single dose of 1 mg ketotifen and 4 weeks treatment of ketotifen, 1 mg twice daily, failed to reduce the methacholine-induced drop in peak expiratory flow. The spirometric findings remained unchanged during ketotifen treatment. There was no difference between treatments with ketotifen and placebo with regard to the patients assessment of the severity of asthma or airway sensitivity to tobacco smoke, fumes or dusts, or exercise. The results suggest that treatment during 4 weeks with ketotifen does not reduce unspecific broncial hyperreactivity in patients with extrinsic asthma.

Adolescent↗
PubMed1980

Comparison of bronchial reactivity to histamine and methacholine in asthmatics.

Eight subjects with asthma underwent bronchial challenge with histamine and methacholine. Dose-response curves were drawn on a scale which made the dosage equivalent in molecular weight. The results were analysed in terms of both the slope of the dose-response curve and the dose required to elicit a 20% fall in FEV1. No significant difference between methacholine and histamine was found in either measurement. Because of the similarity of the responses we conclude that the two agents are similar in action and may be used with equal effectiveness in bronchial challenges.

Adult↗
PubMed1981

The effect of verapamil on histamine and methacholine-induced bronchoconstriction.

Calcium antagonist, verapamil given by inhalation did not alter histamine bronchial hyper-reactivity in ten patients with extrinsic bronchial asthma and similarly did not modify methacholine-induced bronchoconstriction in further five patients. In eight non-asthmatic subjects verapamil reduced histamine sensitivity with increase in PC20H from 8.07(+/- 2.33) to 12.10(+/- 2.71, P less than 0.05) but failed to have an effect on methacholine sensitivity in five controls. The failure of inhaled verapamil to modify histamine and methacholine bronchial hyper-reactivity in asthmatic patients and the beneficial effect of calcium antagonists in exercise asthma suggests that these agents may act predominantly on the mast cell degranulation rather than the bronchial smooth muscle.

Adolescent↗