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A 52-year-old man presented with pure central sleep apnea syndrome that failed to respond to nasal continuous positive airway pressure (NCPAP) therapy. Intermittent positive pressure stimulation via a nasal mask was instituted using a portable positive pressure ventilator. We found marked reduction in the respiratory disturbance index, number of desaturations, and the number of arousals with this mode of therapy.

Chronic asthma and late asthmatic responses (LAR) are associated with local inflammation which might be expected to produce airflow obstruction in small airways and to increase nonspecific airway reactivity. In contrast, early asthmatic responses (EAR) are primarily bronchospastic and probably involve more central airways. We challenged 17 nonsmoking, mildly asthmatic atopic subjects with allergen bronchoprovocation and measured changes in spirometry (FEV1) over the next 24 hours. Each subject also performed a helium-oxygen (He-O2) flow-volume loop before challenge (baseline), during the EAR, and six hours and 24 hours after challenge to measure the effect of gas density on flow rates at midvital capacity. Twelve subjects had both an EAR and a LAR; five subjects had only a LAR. Of these 17 subjects, 15 were initially density dependent, while only two were density independent. During the EAR, 13 percent of the density dependent population had significant decreases in delta Vmax 50 percent; 47 percent had significant decreases during LAR. The He-O2 flow data analyzed at specified time points after challenge revealed significant decreases in the mean delta Vmax 50 percent at six hours in those who had only a LAR (p less than 0.01). In those who had a dual airway response, density dependence increased during the EAR, but decreased at six and significantly at 24 hours (p less than 0.05) postchallenge. There was a strong trend for the severity of the LAR (measured by changes in FEV1) to be directly related to the total decrease in delta Vmax 50 percent during the LAR. We conclude that late asthmatic responses occur frequently after a single antigenic bronchial challenge and can be associated with persistent symptoms. The LAR were often associated with a decrease in density dependence of maximal expiratory airflow, and therefore, may involve small airways.

Pulmonary sarcoidosis is a granulomatous disorder of unknown etiology characterized by both an active cellular immune process and interstitial fibrosis. It has recently been demonstrated that gamma-interferon (the type of interferon associated with an active cellular immune process) is also a potent growth factor for human lung fibroblasts. To evaluate the hypothesis that there is an association between the release of immune interferon and the release of growth factor activity for fibroblasts, bronchoalveolar cells from patients with sarcoidosis were studied for the spontaneous release of both immune interferon and growth factor activity for fibroblasts. Bronchoalveolar cells from 11 of the 24 patients spontaneously released gamma-interferon in vitro. Supernatants from sarcoidosis patients whose bronchoalveolar cells released interferon contained a significantly higher percentage of lymphocytes than those whose bronchoalveolar cell supernatants did not contain interferon (p less than 0.01). Fibroblast growth was also significantly augmented by supernatants from sarcoidosis patients whose bronchoalveolar cells released gamma-interferon compared to supernatants which did not contain interferon (p less than 0.05). In patients with focal abnormalities on chest x-ray films, there was significantly more interferon released by bronchoalveolar cells from the areas that were most abnormal compared to more normal areas of the lung. These studies suggest that there is an association between the release of immune interferon and release of growth factor activity for fibroblasts by bronchoalveolar cells from patients with active pulmonary sarcoidosis.

We employed bronchoalveolar lavage (BAL) of subsegmental airways to study the local inflammatory effects of aeroallergen bronchoprovocation (BPC) and local instillation of allergen in allergic asthmatic patients, allergic rhinitis patients, and normal subjects. Two protocols were used: (1) BAL was performed in three subsegments following BPC or during spontaneous seasonal exposure, and (2) 5-ml aliquots of increasing doses of allergen were instilled into a single subsegment until there was at least 30 percent closure of the airway; the airway was then immediately lavaged. A subsegment in the opposite lung was lavaged as a control site. These same two segments were lavaged again two to 14 days later and the cells and fluid analyzed. Fifty-five lavages have been performed without complications. Pulmonary function tests (FEV1) were not significantly disturbed by either local challenge or lavage procedures. Cells were examined using light and electron microscopy and showed inflammatory cells in alveolar airways and dissolution of mast cell and eosinophil granules. Using selected criteria, we were able to use these methods in mildly, seasonally asthmatic patients to obtain safely cells and fluid for analysis. These techniques may permit studies which further our understanding of the mechanisms responsible for allergic asthma.