The effects of alveolar and pleural pressures on pulmonary interstitial pressure were studied in 36 anesthetized dogs by application of Starling's law of transcapillary exchange. Fluid accumulation in the lung was produced by increasing left atrial pressure to levels always higher than alveolar pressure and by hemodilution with saline. Using a lung divider, a difference in alveolar pressure of from 5 to 14 mm Hg was achieved between the two sides in 24 dogs. Increased alveolar pressure did not reduce the rate of fluid accumulation, indicating its lack of effect on interstitial pressure. A relationship between the rate of fluid accumulation and the forces in the Starling equation was demonstrated when pleural pressure was included as an index of interstitial pressure. The rate of fluid accumulation increased markedly when interstitial pressure exceeded atmospheric. Fluid accumulation was considerably less in lobes statically inflated with plasma than in contralateral lobes ventilated with air (6 dogs); this difference could not be attributed to static inflation as opposed to ventilation (6 dogs). These findings suggest that surface tension opposes the transmission of alveolar pressure to the interstitial space. The interstitial pressure, as measured by application of Starling's law, acts on the small vessels within the alveolar-capillary membrane.
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Mellins et al. (1969) studied this question.
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