Authors: HO Fadnes ( ) , RK Reed ( ) , K Aukland ( )
The present paper deals with the transcapillary fluid balance in hypoproteinemia and increased venous pressure. Interstitial fluid hydrostatic pressure (Pi) was measured by a wick method, and interstitial fluid colloid osmotic pressure (COPi) was measured in tissue fluid samples obtained from implanted wicks. In rat subcutaneous tissue and skeletal muscle the COPi was 10 mm Hg and Pi was -1 mm Hg. In hypoproteinemia a marked fall in COPi was observed in both subcutaneous tissue and skeletal muscle. A fall in plasma COP of 5-6 mm Hg was associated with almost identical fall in COPi. Similar fall in subcutaneous COP was observed by increasing local venous pressure by 10 mm Hg. Raising the venous pressure on the hind limb did, however, not lead to a fall in skeletal muscle COPi in intact, freely moving rats. However, when the hind limb was denervated and immobilized an increase of venous pressure caused a fall in skeletal muscle COPi, similar to that observed in subcutaneous tissue. In both hypoproteinemia and increased venous pressure no rise in Pi could be measured before visible edema was detected. The results indicate that the fall in COPi will prevent or limit edema formation in hypoproteinemia and when the venous pressure is increased. In addition, in skeletal muscle the muscle pump will protect against increased capillary fluid filtration when the venous pressure is increased, probably by keeping a low capillary pressure during muscle contractions.
How to Cite: Fadnes, H. , Reed, R. & Aukland, K. (1978) “MECHANISMS REGULATING INTERSTITIAL FLUID VOLUME”, Lymphology. 11(4).