Surface activity of sputum from acute asthmatic patients.

K Kurashima, M Fujimura, T Matsuda… - American journal of …, 1997 - atsjournals.org
K Kurashima, M Fujimura, T Matsuda, T Kobayashi
American journal of respiratory and critical care medicine, 1997atsjournals.org
The cause of airway resistance that develops during an asthma attack is not fully
understood. Besides bronchospasm and airway edema, a surfactant dysfunction has been
suggested as a reason for an increase in airway resistance. This study sought to determine if
surface activity of airway fluid is altered in acute asthmatic attacks. Sputa were collected
serially from seven patients with acute asthmatic attacks and compared with that of normal
subjects (n= 15) and subjects with stable asthma (n= 14). Sputa were analyzed for minimal …
The cause of airway resistance that develops during an asthma attack is not fully understood. Besides bronchospasm and airway edema, a surfactant dysfunction has been suggested as a reason for an increase in airway resistance. This study sought to determine if surface activity of airway fluid is altered in acute asthmatic attacks. Sputa were collected serially from seven patients with acute asthmatic attacks and compared with that of normal subjects (n = 15) and subjects with stable asthma (n = 14). Sputa were analyzed for minimal surface tension (STmin), phospholipids (PL), and total proteins (TP). There were no significant differences in STmin, PL, and TP between sputa from normal subjects and subjects with stable asthma. In the acute phase of the attack, TP, TP/PL ratio, and STmin significantly increased. However, in the recovery phase of the attack, TP/PL ratio and STmin significantly decreased. These data demonstrated that surface properties of airway fluid deteriorated in the early phase of the asthma attack, but were ameliorated in the recovery phase possibly by the surfactant recruitment. The drastic changes in surface activity of sputum suggest that changes in airway surfactant may be partly involved in the pathogenesis of the airway obstruction during asthmatic attack.
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