With the aim of determining the structural conditions which affect fluid movement in the cutaneous connective tissue of mice, various test fluids were brought into contact with it under conditions such that neither blood vessels nor lymphatics were directly entered. Locke's solution, mouse serum, and a mixture of Locke's solution with a dye which causes edema were all employed. At atmospheric pressure, Locke's solution entered the tissues intermittently. When subjected to very low pressures it continued to enter the skin intermittently and at approximately the same rate. At pressures above 4.5 cm. of water, however, the flow became continuous but it did not increase in rate significantly until pressures of about 8.5 cm. were employed. There was no relationship between the rate of flow and the pressure employed. At a pressure of about 8.5 cm. the resistance of the tissues seemed to give way abruptly as if the formed elements had been separated. This has been termed the "breaking point." After it had been reached each further increase of pressure produced a proportionately greater inflow.
Under the conditions of our experiments, the dye-Locke"s solution and also the homologous serum failed to enter the tissues at atmospheric pressure. It was necessary to subject these fluids to pressure to force them into the skin at the same rate at which the Locke's solution entered it spontaneously. Under these circumstances the dye-Locke's solution and the serum entered the skin continuously, not intermittently like the plain Locke's solution. As the pressure was gradually raised, no significant increase of flow into the tissues occurred until a point was reached, on the average 8.5 cm. of water, at which fluid suddenly began to enter very rapidly. This point, the "breaking point" already mentioned, was reached at the same pressure irrespective of the character of the fluid employed, showing that the phenomenon was produced by the fluid bulk. Once it had been attained, further increases in pressure caused proportionately greater inflow of fluid. The circulation had nothing to do with the phenomenon, for it occurred in the skin of dead mice."
The findings indicate that under normal circumstances the movement of fluid in the interstitial tissue does not take place as though in preexisting channels. The experiments confirm previous observations from this laboratory (13, 14) that in normal skin tissue the state of affairs is such that fluid cannot flow freely. However, when fluid is introduced into the skin under pressure spaces are forcibly opened up.
Inflammatory edema in the skin changed the phenomena of fluid entrance into it under pressure. The reason is that there then occurred a separation of the formed elements and the interstitial fluid moved as in preformed channels. Even when very low pressures were employed (3.0 to 7.0 cm. of water), there appeared usually a linear relationship between the pressure and the rate of flow.