A small atmospheric bubble was introduced into a surfactant suspension
in a captive bubble surfactometer. After film formation to the equili
brium surface tension at the bubble air-liquid interface, the bulk pha
se surfactant was depleted by replacing the chamber contents several t
imes with a saline-CaCl2 solution. The remaining film adsorbed at the
bubble surface was then compressed stepwise in quasi-static fashion to
near zero minimum surface tension. This was followed by a series of q
uasi-static expansion steps to surface tensions slightly above equilib
rium. The surface tension of films from lipid extract surfactants and
phospholipid mixtures did not increase in a manner consistent with the
presence of a single surface monolayer. After the initial, rapid rise
in surface tension at each expansion step, a decrease in surface tens
ion to a new value was observed. This decrease in surface tension is l
ikely due to the adsorption of 'surplus' material from a 'surface-asso
ciated reservoir' into the surface active film. The presence of surplu
s non-monolayer surfactant material in situ at the alveolar surface wa
s also demonstrated by electron microscopy. SP-A acted as a potent pro
moter for the movement of excess material (equivalent to 2-3 monolayer
s) at the interface into the surface active film. In contrast, inhibit
ory serum proteins prevented the formation of a surface-associated res
ervoir or the adsorption of excess material into a surface active film
.