In considering the formation of pulmonary oedema it is usual to apply Starling's hypothesis (Starling, 1894). This states that the rate of passage of fluid across capillary endothelium is proportional to the difference between the hydrostatic pressure across the membrane (tending to produce oedema) and the transmural colloid osmotic pressure drop (tending to resolve oedema). Applied to the lungs it is often supposed that the hydrostatic and colloid osmotic pressures in the alveolar walls are negligible, so that when the capillary blood pressure exceeds the colloid osmotic pressure of the blood (about 25-30 mm Hg), fluid passes across the capillary wall; it is not known if these assumptions are valid. Furthermore, the distensibility of the pulmonary vascular bed must be considered. A rise in capillary blood pressure will increase the rate of transudation of fluid not only by the change in hydrostatic pressure but also by increasing the area and decreasing the thickness of the alveolar-capillary membrane.We have tried to determine a permeability coefficient for rabbits' pulmonary capillaries, as has been done by Landis (1927) for the mesenteric capillaries of the frog, and by Pappenheimer & Soto-Rivera (1948) for the circulation of the cat's leg. Our results have led us to consider how Starling's hypothesis can best be applied to the pulmonary circulation, and to an investigation of the forces involved in the transudation of fluid across the capillaries of the lung.
METHODSThe principle of the method was to perfuse rabbit lungs with blood while controlling the perfusion pressure and measuring the rate of formation of oedema fluid. The rabbits used weighed from 2-0 to 2-4 kg.Perfu8ion method. The perfusion pump was designed to give non-pulsatile flow of blood with a small difference of pressure (2-4 mm Hg) between pulmonary artery and veins; this was to allow
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