MECHANISMS REGULATING INTERSTITIAL FLUID VOLUME

Abstract

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 (COP_i) was measured

in tissue fluid samples obtained from implanted

wicks. In rat subcutaneous tissue and skeletal muscle

the COP_i was 10 mm Hg and Pi was -1 mm Hg. In

hypoproteinemia a marked fall in COP_i 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 COP_i 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 COP_i, 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 COP_i 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.