The calcium-dependent constriction of bronchial smooth muscle cells and release of mediators derived from mast cells is important in the pathophysiology of asthma. We hypothesized that nifedipine, a slow calcium channel blocker, would inhibit or attenuate acetylcholine-induced bronchoconstriction in asthmatics. Because one consequence of mast cell activation is the release of platelet-activating factor, we wondered whether thromboxane levels would be increased during acute bronchial constriction in asthmatics. Bronchoconstriction was induced in 8 asthmatics (6 men, 2 women) by acetylcholine; each subject was pretreated either with placebo or nifedipine (20 mg sublingually) on 2 separate days. Vital capacity, forced expiratory volume in 1 s, peak expiratory flow rates and oscillatory resistance were measured prior to and after the intake of placebo or nifedipine as well as after an acetylcholine challenge. Pretreatment with nifedipine significantly attenuated acetylcholine-induced changes in all four lung function parameters studied, but did not significantly influence the increase in thromboxane B2 plasma concentrations observed after the acetylcholine challenge. From these data we conclude that nifedipine inhibits the acetylcholine-induced bronchoconstriction in asthmatics. This effect may be either a direct action on bronchial smooth muscle or may be due to the inhibition of mediators other than thromboxane.
The acute effects of a single intravenous Prostigmin injection (0.5 mg) on lung function and gas exchange during rest and bicycle ergometry were measured in 26 patients with myasthenia gravis. The mean age of the patients was 44.6 ± 17.6 years and the mean duration of myasthenia gravis 5.4 ± 6.3 years. Lung function parameters obtained from 15 patients showed a normal total lung capacity with an increase in functional residual capacity and residual volume, while vital capacity was diminished. While the application of Prostigmin showed no acute effects on these lung volumes, there was a significant increase in airway resistance, even into the pathologic range. Data obtained during spiro-ergometry concerning gas exchange, circulation and muscle metabolism correspond to those expected from healthy individuals; application of Prostigmin did only influence the heart rate, which can be explained by parasympathomimetic activity. We conclude that dyspnoea in patients with myasthenia gravis need not necessarily be a symptom of the illness itself but can also be caused by therapy; in the latter case bronchodilatators are required
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