Bronchoconstriction elicited by the inhalation of ultrasonically nebulized distilled water’ is presumed to be at least partly provoked by a nonimmuno-logic release of mediators from mast cells in the airways. Recent evidence has suggested this hypothesis. In fact, circulating concentrations of the mast cell-associated mediators, histamine and neutrophilic chemotactic factor, increase in asthmatic subjects after inhalation of ultrasonically nebulized distilled water. This accompanies the development of distilled water-induced asthma in a way analogous to the increase in both mediators observed after antigenic challenge. Disodium cromoglycate, a mast-cell stabilizer, can modify the asthmatic response to inhaled ultrasonically nebulized distilled water as it modifies the early reaction to inhalation of allergen.
Finally, the hypo-osmolarity of the aerosol seems to be an important determinant of bronchoconstriction induced by ultrasonically nebulized distilled water, and it has been demonstrated that mast cells in vitro can release histamine in hypotonic solutions. Transient changes in the osmolarity of the fluid surrounding mast cells in the airways may be all that is required to induce release of mediators and contraction of smooth muscles, either directly or via the vagus nerve.
Black et al have recently demonstrated that inhalation of ultrasonically nebulized distilled water can induce an increase in nonspecific bronchial responsiveness as allergenic exposure does. This might provide further evidence that there are some common mechanisms in asthma induced by distilled water and in asthma induced by inhalation of allergens.
Nevertheless, some questions arise about this point. In fact, it is well known that the increase in bronchial responsiveness elicited by allergenic exposure is generally associated with the occurrence of late reactions, and although the factors provoking these two phenomena remain unknown at present, inflammation and the release of mediators from pulmonary cells or from cells migrated during the inflammatory response seem to be involved. By contrast, no late asthmatic response to inhaled ultrasonically nebulized distilled water has been reported in asthmatic subjects, and at present, there is no evidence demonstrating that the time course of such a water-induced increase in bronchial hyperresponsiveness is similar to that observed after inhalation of allergens.
We have recently noticed that some of the subjects who were taking part in a separate study of asthma induced by ultrasonically nebulized distilled water complained of wheezing several hours after the inhalation. In the present study, we therefore investigated the occurrence of any late asthmatic response after inhaled ultrasonically nebulized distilled water and the time course of any change in responsiveness to methacholine induced by this stimulus.
This might have clinical relevance because the inhalation of distilled water seems to stimulate a naturally occurring stimulus (foggy weather) in asthmatic patients, and challenge with ultrasonically nebulized distilled water has been proposed as an alternative method to measure bronchial responsiveness.
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