Peritoneal transport physiology: insights from basic research.

Abstract

Clinical uses of the peritoneal cavity, such as i.p. chemotherapy or peritoneal dialysis, depend on underlying physiological mechanisms of transport between the blood and the peritoneal cavity. Clinical models of peritoneal transport have focused on an idealized "peritoneal membrane." However, such a membrane does not physically exist. Transport actually occurs between the peritoneal cavity and blood which is contained in discrete capillaries distributed in the tissue interstitium surrounding the cavity. To integrate the properties of the capillaries and the interstitium, the "distributed model" approach couples pore theory, which simulates transendothelial transport, with diffusion and convection within the tissue space. The distributed theory can explain why the peritoneal membrane, when compared with the artificial kidney, appears tight to urea but leaky to protein. The additional resistance to urea transport has been attributed to "unstirred layers" adjacent to the peritoneal membrane. These can now be defined physiologically by examining diffusion in the tissue space. Absolute rates of convection into and out of the cavity cannot yet be accurately predicted, but the physiological forces can be specified. Net "ultrafiltration" during dialysis results from not only high osmotic pressure in the peritoneal dialysate but also from a small but significant hydrostatic pressure which drives convection in the opposite direction. Recent implications from protein absorption studies that lymphatics are the cause of the decrease in net ultrafiltration are only partly true. Analysis of data from the tissue space has shown that the deposition of protein occurs from the cavity into the tissue interstitium with a slow uptake into lymphatics.