Transcapillary transport after thermal injury.

The pathophysiology of the burn wound is characterized by an inflammatory reaction leading to rapid edema formation due to (1) dilatation of resistance vessels with increased effective transcapillary filtration pressure, (2) increased extravascular osmotic activity created in damaged tissue, and (3) increased microvascular permeability to macromolecules. In extensive burns increased microvascular permeability was found also in tissues remote from the thermal injury. These reactions are due to direct heat effect on the microvasculature and to chemical mediators of inflammation. Important is the increased biosynthesis of prostaglandins at the site of tissue injury which may partly explain vasodilatation, increased microvascular permeability and accumulation of polymorphonuclear leucocytes observed following thermal injury. The morphological interpretations of the changes in the functional ultrastructure of the blood-lymph barrier following thermal injury seem to be a remarkable and persistant increase in the numbers of vacuoles and many open endothelial intercellular junctions. Further less explored changes of the interstitial tissue after severe burn trauma seem to be of great importance.