Rationale: African Americans acutely ill with asthma come to emergency departments more frequently and are admitted to hospital more often than whites but the reasons are unclear. Objectives: To determine whether such phenomena represent racial differences in attack severity or limited effectiveness of  2 -agonist therapy. Methods and Main Results: We contrasted clinical features, airflow limitation, and albuterol responsiveness in adults acutely ill with asthma, 155 of whom where African American and 140 white, as they presented to eight emergency departments. Assessments were standardized across institutions using a care path, and admission and discharge decisions were made according to predetermined criteria. The degree of obstruction was measured by peak expiratory flow rates. The clinical features of both groups were similar. The African Americans, however, had lower flow rates (p ϭ 0.002), and more of them experienced severe or potentially life threatening episodes (p Ͻ 0.001). Albuterol was equally efficacious in both populations and there were no differences in the post-treatment flow rates achieved irrespective of the initial attack intensity. There were no racial differences in admission/discharge ratios. Conclusions: Our data indicate that African Americans with asthma tend to present with somewhat more intense attacks than whites, but they respond equally well to routine treatment. Similarly, there were no racial disparities in hospitalizations when standard criteria are employed.
To determine the effect of hyperpnea on the characteristics of periciliary liquid, we collected airway surface fluid (ASF) and measured its osmolarity in 11 normal people while they breathed dry, frigid air (-17 +/- 1.2 degrees C) at minute ventilations (VE) of 10, 40, and 80 l/min through a heat exchanger. The ASF was collected at the fifth tracheal ring by absorption onto filter paper pledgets inserted via fiber-optic bronchoscopy. Hyperpnea had no influence on the amount of ASF recovered (ASF volume at a VE of 10 l/min = 12.0 +/- 2.0 microl; at 80 l/min = 8.8 +/- 1.5 microl; P = 0.28) or its osmolarity (at a VE of 10, 40, and 80 l/min = 326 +/- 15, 323 +/- 11, and 337 +/- 12 mosM, respectively; P = 0.65). These findings demonstrate that the tracheal mucosa of normal subjects does not dessicate during hyperpnea and that hypertonicity of the periciliary fluid does not develop even at high levels of ventilation.
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