[Airway reaction of patients with bronchial asthma breathing sulfur dioxide].
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Biomedical subjects
Publications and source records attributed to H Magnussen.
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UNLABELLED: The bronchodilator effect of a single dose of 0.4 mg fenoterol aerosol was compared with the sequential application of the same total dose in 11 patients with bronchial asthma. The patients received either 0.4 mg fenoterol followed by 3 doses of placebo at 30 minute intervals or four 0.1 mg doses of fenoterol each at 30 minute intervals on 2 days in a double-blind randomised investigation. Both application forms had a marked bronchodilator effect. At 60 minutes two 0.1 mg doses of fenoterol had the same effect as the initial dose of 0.4 mg whereas at 120 minutes the sequential inhalation of 0.1 mg had the most marked bronchodilator effect. CONCLUSION: An improvement in beta 2-sympathomimetic inhalation therapy can be achieved more readily by reducing the dose interval than by raising the total dose.
In haemodialysis patients Staphylococcus aureus is the most frequent pathogen in infections of vascular access. At the same time, a very high share of these patients (up to 55%) are Staphylococcus aureus carriers. Hygienic measures during puncture of the shunt are highly important for prevention of shunt infection which is most likely endogenous.
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In patients with respiratory failure, almitrine causes an increase in arterial O2 partial pressure (paO2) by stimulating peripheral chemoreceptors. Since such patients often require long-term O2 therapy inhibiting peripheral chemoreceptor activity, the effect on arterial blood gases by almitrine (100 mg orally) and increasing amounts of nasally supplied O2 was studied. In ten patients with severe chronic airways obstruction and pulmonary emphysema, almitrine produced a mean increase of paO2 by 5.2 mm Hg both while breathing normal air and during nasal administration of O2 (0.5-2.0 l/min), whereas paCO2 levels remained constant. In 4 patients with pulmonary fibrosis almitrine did not change the paO2. These results show that patients with chronic airways obstruction and pulmonary emphysema respond to a single dose of 100 mg almitrine by an increase of paO2 equivalent to that achieved by administering 1.0 l/min of O2 via the nose.
Plasma cell granuloma is a rare, benign and usually solitary round tumour of the lung. Although uncommon, it is found relatively more frequently among children and adolescents. The lack of symptoms and absence of characteristic features make diagnosis difficult. In adults, the differentiation from bronchial carcinomas is particularly difficult because of their radiological similarity. Consequently, thoracotomy and excision of the tumour is the treatment of choice.
Recently, several transmembrane calcium-channel blockers have been used in experimental models to investigate the mechanisms through which Ca++ ions contribute to the regulation of the contractile response of airway smooth muscle and to determine the therapeutic use of these drugs in bronchial asthma. Since the data from these studies are inconsistent and inconclusive, we studied the effect of diltiazem, a calcium-channel blocker previously not examined to our knowledge, on histamine- and carbachol-induced bronchoconstriction in healthy and in asymptomatic allergic bronchial asthma. The study was performed in a double-blind, randomized, placebo-controlled fashion, using a single oral dose of 60 mg of diltiazem. Airway reactivity to histamine and carbachol expressed by PD35SGaw was significantly but weakly attenuated by diltiazem in the asthmatic, but not in the normal subjects. Baseline lung function was not significantly influenced by diltiazem. We concluded that the effect of diltiazem on unspecific airway hyperresponsiveness in asthmatic subjects is too weak to justify a recommendation as therapy.
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The bronchoconstrictor response to cold air breathing during exercise shows a wide interindividual variation in asthmatic patients. We investigated whether the protective effect of a single, inhaled dose of 0.2 mg fenoterol powder is dependent on the severity of airways obstruction, following placebo pretreatment of an inhalative thermal burden precisely matched in terms of respiratory heat exchange. In ten asthmatic patients 0.2 mg fenoterol powder or placebo were administered via an inhalator in a single blind and random order fashion on separate days. Lung function was measured before and 30 min after treatment (baseline value) and 3, 10, 15 and 30 min after an inhalative provocation consisting of cold air breathing during exercise. After placebo the maximal increase of airway resistance compared to the baseline value ranged from 682% to 50% (means +/- SD: 344.1 +/- 312.2) whereas fenoterol shifted the corresponding data to 58% and -23.0% (means +/- SD: 13.4 +/- 29.2). The protective effect of fenoterol did not depend on the reactivity of the airways to the stimulus applied. The results indicate that the inhalative pretreatment with 0.2 mg fenoterol powder is sufficient to block exercise-induced asthma even in those patients whose airways are highly sensitive to respiratory heat loss.
Thirty patients (27 men and 3 women) with an average industrial asbestos exposure of 19 years have been examined. The results of conventional radiography and CT have been analysed and compared with pulmonary function studies. The advantages of CT depend on a better demonstration of the pleura and lung periphery. In 24% of cases plaques were diagnosed by chest x-rays which could, however, be excluded by computed tomography. Correct prediction of restricted ventilation was possible in 84% patients by means of CT. On the other hand, this prediction by means of conventional radiographs could be made reliably only if there was extensive fibrosis.
Since the calcium antagonists nifedipine and verapamil have been shown to diminish exercise induced asthma, the effect of oral diltiazem, a calcium channel blocker not previously investigated in this context, was studied. Ten patients with bronchial asthma were given 60 mg diltiazem or placebo four hours before the challenge in a double blind, randomised, crossover fashion. Exercise was performed on a cycle ergometer while the subjects were breathing cold air, resulting in a respiratory heat exchange which was similar at the two study sessions. FEV1 and specific conductance (sGaw) were recorded before and three, 10, 15, and 30 minutes after the challenge. No significant differences were found between placebo and diltiazem days in the fall of FEV1 or sGaw after exercise. Thus unlike other calcium antagonists diltiazem, in a dose of 60 mg given orally four hours before exercise, failed to protect against exercise induced asthma.
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We investigated the modification of histamine-induced bronchoconstriction by the H2-antagonist cimetidine in conscious sheep. One hundred breaths of 5% histamine aerosol increased mean (SD) pulmonary resistance (RL) by 5.6 (1.4) cmH2O/l/sec. This increase in RL was completely blocked by intravenous clemastine (0.5 mg), a specific H1-antagonist, indicating that the histamine-induced bronchoconstriction was mediated by H1-receptors. Intravenous cimetidine caused a dose-dependent enhancement of the histamine response between 1 and 1000 mg with a mean peak delta RL of 15.3 (5) cmH2O/l/sec (p less than 0.05) at the 1000 mg dose, while it blocked the histamine response at a dose of 2400 mg [delta RL = 1.9 (2) cmH2O/l/sec, p = NS]. This paradoxic effect was not related to an anticholinergic mechanism as intravenous cimetidine (2400 mg) failed to block carbachol-induced (25 breaths of 1% solution) bronchoconstriction. We conclude that in the ovine airway, cimetidine is a selective H2-histamine receptor blocker at lower tissue concentrations, and a combined H2- and H1-histamine receptor blocker at high tissue concentrations.
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