Recent studies have found that severe
surfactant dysfunction occurs during an
asthma attack, but the changes in
surfactant in a guinea-pig model of chronic
asthma have not been studied. We therefore analysed the
surfactant recovered from guinea-pigs after repeated inhalation of
ovalbumin to see if the
surfactant recovered from chronic asthmatic lungs would be intrinsically altered. Guinea pigs immunized through repeated inhalation of aerosolized
ovalbumin (OA) were exposed to the
antigen once a week for a month. Twenty-four hours after the last challenge the alveolar wash was recovered. We calculated saturated
phosphatidylcholine (Sat-PC) and total
protein (TP) pool sizes in alveolar spaces.
Surfactant subtype conversion of large aggregate
surfactant (LA) to small aggregate
surfactant was studied in vitro by means of the surface area cycling technique. The
phospholipid composition of LA was analysed by thin layer chromatography and the surface activity of LA was also determined. We found decreased
surfactant pool sizes, decreased ratio of Sat-PC to TP in alveolar lavages in
asthma groups, and surface activity of the
surfactant recovered from asthmatic lungs to be inferior to that of the controls. Accelerated
surfactant subtype conversion in vitro was also noted in the lungs of asthmatic animal models. In addition, the changes in
phospholipid compositions which were similar to the pattern of
acute lung injury suggested that alveolar
inflammation might be involved in the pathogenesis of chronic
asthma. These results indicate that
surfactant is intrinsically abnormal in chronically asthmatic lungs.