Background: Dopamine exerts inhibitory and excitatory effects on different systems. In the lungs, dopamine modulates respiratory functions through carotid bodies and modulates pulmonary blood vessel tone, alveolar liquids, and bronchial exchange, and possibly participates in the regulation of airways diameter. It has been reported that dopamine has no acute effect on human airways in normal subjects or those with asthma background. However, inhaled or infused dopamine decreased histamine-induced bronchoconstriction in both normal and asthmatic subjects. We have examined the possible modulating effect of dopamine on bronchial diameter by administering inhaled dopamine and the DA2 dopaminergic blocker metoclopramide to subjects with various degrees of bronchial tone.
Methods: We examined 56 volunteers. Arterial blood pressure and heart rate were determined in every subject. By means of spirometry, we measured forced vital capacity, forced expiratory volume in the first second, maximal forced expiratory flow, and forced expiratory flow at 50% of vital capacity, before and after each treatment. By inhalation with a nebulizer, we administered dopamine (0.5 microg/kg/min) to 10 healthy subjects, 10 subjects with asthma without acute bronchospasm, and 16 subjects with acute asthma attack; intravenous metoclopramide (7 microg/kg/min) was administered to 10 healthy subjects and 10 subjects with asthma without acute bronchospasm. For ethical reasons, metoclopramide was not used in subjects with acute asthma attack.
Statistics: non-parametric Wilcoxon tests for paired samples, ANOVA tests, and Bonferroni multiple comparison tests were performed.
Results: Inhaled dopamine increased forced expiratory volume in the first second, forced vital capacity, maximal forced expiratory flow, and forced expiratory flow at 50% of vital capacity in the acute asthma attack group, but there were no modifications in the healthy group or in the asthma without acute bronchospasm group. Metoclopramide did not induce changes in respiratory parameters in healthy individuals or in those with asthma without acute bronchospasm.
Conclusions: Inhaled dopamine was able to induce bronchodilatation when the bronchial tone was already increased by acute asthma attack, but it did not modify the resting bronchial tone in normals or in asthmatics without acute bronchospasm. DA2 blockade with metoclopramide did not modify resting bronchial tone either. We suggest that dopamine exerts a modulatory effect on bronchial tone of human airways depending on the degree of existing basal tone.