1 delta1‐trans‐tetrahydrocannabinol, (delta1‐THC) produces bronchodilatation in asthmatic patients. 2 Administered in 62 microliter metered volumes containing 50–200 microgram by inhalation from an aerosol device to patients judged to be in a steady state, it increased peak expiratory flow rate (PEFR) and forced expiratory volume in 1 second (FEV1). 3 The rate of onset, magnitude, and duration of the bronchodilator effect was dose related.
(1978). Thorax, 33, 479482 Bronchodilatation after inhalation of the antihistamine clemastine. H, receptor blocking antihistamines administered by mouth have not found a clear place in the management of bronchial asthma. We investigated the possibility that higher concentrations of these drugs, administered directly to the bronchial tree, might produce bronchodilatation.Twelve asthmatic patients inhaled aerosols generated from solutions of clemastine (0 05%0), salbutamol (0 5%), and placebo. Bronchodilatation was assessed by changes in the forced expiratory volume in one second (FEVY) and peak expiratory flow rate (PEFR) over four hours.Both clemastine and salbutamol caused significant bronchodilatation. The mean maximum percentage increases in FEV, for clemastine and salbutamol were 21 1 % and 29 2% respectively. The mean maximum percentage increases in PEFR were 31-2% and 35-2% respectively. There was no significant difference in the maximum bronchodilatation produced by the two drugs.Clemastine, when administered by aerosol inhalation, appears to be an effective bronchodilator.The role of histamine in the production of acute asthma is controversial. There is evidence that histamine is released in allergic reactions in the lung (Schild et al, 1951), and challenge studies have shown that the bronchi of asthmatics are more sensitive to histamine than those of nonasthmatics (Curry, 1947;Tiffenau, 1958;Townley et al, 1965). Oral antihistamine drugs have not found a place in treating asthma, however, and are widely thought to be ineffective (Lancet, 1955).Assuming that histamine plays a role in asthma, the therapeutic failure of antihistamines could be due either to the failure to block the H2 receptor sites or to incomplete H, receptor blockade caused by inadequate local concentrations of drugs. Indeed, higher doses of antihistamines, given by mouth or parenterally, have caused bronchodilatation (Popa, 1977), but central nervous system depression limits their use by this route.We have attempted to assess whether the administration of an H, receptor blocking antihistamine, clemastine, given directly to the bronchi as an aerosol, could cause therapeutically useful bronchodilatation. PatientsTwelve patients (age range 29-70, mean 46) gave informed consent. All were in hospital having recovered from a severe exacerbation of bronchial asthma and were in a relatively stable clinical state. All had previously shown reversibility of airways obstruction by a greater than 15% increase in peak expiratory flow rate (PEFR) after inhaling salbutamol aerosol 200 ,ug. Six of the twelve patients were atopic by prick skin testing. On three consecutive mornings each patient had baseline measurements of PEFR (the best of three recordings) using a Wright peak flow meter and forced expiratory volume in one second (FEV1) using a dry wedge spirometer (Vitalograph). Each subject then inhaled from a Wright's nebuliser 1 ml each of either clemastine 0-05% in saline, salbutamol 0 5%, or physiological saline as 479 on 10 May 2018 by guest....
An episode of exercise induced asthma will usually be followed by a period during which further exercise will not induce asthma. Postulated mechanisms include persistence of catecholamines released during exercise, development of tolerance to released mediators, and mediator depletion. To investigate the underlying mechanism further eight asthmatic men underwent three experimental protocols as follows: two treadmill runs of eight minutes; two incremental challenges with histamine inhalation; and a treadmill run of eight minutes followed by an incremental challenge with histamine inhalation. In each case the two challenges began 40 minutes apart. Patients performed the paired exercise trial first. Refractoriness to bronchoconstriction was shown in the repeated exercise studies but did not occur with repeated histamine challenge. The geometric mean histamine concentrations required to produce a 20% fall in forced expiratory volume in one second (FEV,) were 1*53 mg/ml and 093 mg/ml for the first and second challenges respectively (NS) and 1-4 mg/ml (NS) for the histamine challenge after exercise. It is concluded that refractoriness to exercise induced asthma is not explained by the development of smooth muscle tolerance to repeated histamine exposure or by the persistence of catecholamines released during exercise. The data are consistent with the theory of mediator depletion as the cause of refractoriness.
The bronchodilator effects of inhaled dry salbutamol powder (50, 100, 200 and 400 μg) have been compared in ten asthmatic patients with those of aerosolized salbutamol (200 μg) delivered from a standard pressurized inhaler. A dose of salbutamol powder (400 μg) produced greater bronchodilatation than 50, 100 or 200 μg of powder, but there was no significant difference between 400 μg of powder and 200 μg of aerosolized salbutamol. Powder administered by Rotahaler is well tolerated and offers several advantages over the pressurized aerosol canister.
The ability of the Hi receptor antagonist clemastine to prevent exercise-induced asthma (EIA) has been studied in 10 adult asthmatic subjects. Exercise was performed for eight minutes on a cycle ergometer on two occasions on each of two days. The viously been shown to have exercise-induced asthma (fall in peak expiratory flow rate, PEFR, or forced expiratory volume in one second, FEV, of > 15% after exercise).Patients performed two exercise tests separated by two hours on each of two study days. The initial test on each day was used to confirm that a similar degree of exercise asthma was present. If the fall in PEFR or FEV1 was <15% after the first test, the subject was asked to attend on another occasion, or was withdrawn from the study. If, in addition, at the second visit, the fall in PEFR or FEV1 differed by more than 15% from that at the first, then that individual's response to exercise was considered too variable and he was not included in the study.Ten patients were considered to have reproducible EIA by the criteria outlined above, and their results form the basis of this report. Their mean age was 35 years (range 24-45 yr) and six were male. Nine patients had positive skin prick tests to two or more common allergens. No drugs were permitted within 12 hours of exercise testing, with the exception of oral or inhaled corticosteroids (four patients). No patient had taken antihistamines within four weeks of the study.
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