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The influence of volume changes and interfacial forces on the geometry of peripheral air spaces was studied in excised rabbit lungs inflated with either air or saline and fixed by vascular perfusion at four points of the deflation limb of the pressure-volume curve corresponding to 100, 80, 60, and 40% of the total lung capacity (TLC). In air-filled lungs pleating and folding of alveolar septa were observed, especially in alveolar corners. However, the alveolar surfaces were smooth, except at low lung volumes where some surface crumpling occurred. In saline-filled lungs pleats were absent; the alveolar surface was irregular at all inflation levels due to undulating walls and bulging capillaries. Morphometry indicated that at all alveolar volumes (VA) the surface areas (SA) were larger in saline- than air-filled lungs. No simple mathematical function was found to characterize the relation between SA and VA over the entire volume range studied. Within the range of normal breaths (80 to 40% TLC) the best fit for n in the function SA = k.VnA was 0.58 for saline-filled lungs (r = 0.93) and 0.33 for air-filled lungs (r = 0.68), suggesting different and complex deflation patterns.

For pulmonary structure-function analysis excised rabbit lungs were fixed by vascular perfusion at six points on the pressure-volume (P-V) curve, i.e. at 40, 80, and 100% of total lung capacity (TLC) on inflation, at 80 and 40% TLC on deflation, and at 80% TLC on reinflation. Before fixation alveolar surface tensions (gamma) were measured in individual alveoli over the entire P-V loop, using an improved microdroplet method. A maximal gamma of approximately 30 mN/m was measured at TLC, which decreased during lung deflation to about 1 mN/m at 40% TLC. Surface tensions were considerably higher on the inflation limb starting from zero pressure than on the deflation limb (gamma-V hysteresis). In contrast, the corresponding alveolar surface area-volume (SA-V) relationship did not form a complete hysteresis over the entire volume range. There was a considerable difference in SA between lungs inflated to 40% TLC (1.49 +/- 0.11 m2) and lungs deflated to 40% TLC (2.19 +/- 0.21 m2), but at 80% TLC the values of SA were essentially the same regardless of the volume history. The data indicate that the gamma-SA hysteresis is only in part accountable for the P-V hysteresis and that the determinative factors of alveolar geometry change with lung volume. At low lung volumes airspace dimensions appear to be governed by an interplay between surface and tissue forces. At higher lung volumes the tissue forces become predominant.

We tested a new captive bubble surface tensiometer with films adsorbed from aqueous suspensions of rabbit lung surfactant and a bovine lung surfactant lipid extract and with films of dipalmitoyl-sn-3-glycerophosphorylcholine (DPPC) spread from solvents. The lack of tubes penetrating the bubble surface eliminated potential leakage pathways for the surface film, which was compressed by increasing external pressure. Surface tensions and areas were calculated directly from bubble shapes without the need of pressure measurements. After only one to two compressions, the rabbit surfactant films exhibited the low surface tension, collapse rates, and compressibilities characteristic of the alveolar surface in situ and approached the behavior of spread DPPC films. The bubble "clicking" phenomenon described earlier by Pattle (Proc. R. Soc. Lond. B Biol. Sci. 148: 217-240, 1958) was also reproduced, but only with the bovine extract, which did not perform as well as the rabbit surfactant in surface tests. These findings suggest that surfactant apoprotein SP-A, which was probably present in the rabbit but not the bovine preparations, enhances both adsorption and stability of pulmonary surfactant monolayers.

A small atmospheric bubble was introduced into a surfactant suspension in a captive bubble surfactometer. After film formation to the equilibrium surface tension at the bubble air-liquid interface, the bulk phase surfactant was depleted by replacing the chamber contents several times 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 quasi-static expansion steps to surface tensions slightly above equilibrium. 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 tension to a new value was observed. This decrease in surface tension is likely due to the adsorption of ‘surplus’ material from a Ê»surface-associated reservoir’ into the surface active film. The presence of surplus non-monolayer surfactant material in situ at the alveolar surface was also demonstrated by electron microscopy. SP-A acted as a potent promoter for the movement of excess material (equivalent to 2-3 monolayers) at the interface into the surface active film. In contrast, inhibitory serum proteins prevented the formation of a surface-associated reservoir or the adsorption of excess material into a surface active film.

The appearance of the microstructure of the lung as revealed in transmission and scanning electron micrographs of perfusion-fixed air- and saline-filled lungs suggests the following model for the structure of the alveolar duct. There are two networks of force-bearing elements. The first is an interdependent part of the peripheral connective tissue system that starts from the pleura and extends into the interlobar and interlobular fissures. At the sublobular level, its geometry is not yet fully clear. This network is extended by changes in lung volume and is insensitive to surface tension. The second network is composed of the line elements that form the rims of the alveolar openings. This network is the terminal part of the axial fiber system that surrounds bronchi, bronchioli, and arteries. The line elements of this network are extended by the outward force of surface tension. The two-dimensional alveolar walls that form the alveoli are negligible mechanical components except as platforms for surface tension at the air-liquid interface. An analysis of the mechanics of this model yields relations among surface area, recoil pressure, lung volume, and surface tension that are consistent with published data for lung volumes below 80% of total lung capacity.

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