Permeability of blood vessels after thermal injury

The permeability of the microcirculation in the canine mesentery, following heat stresses and topical application of histamine, was studied by introducing directly into the mesentric circulation albumin or dextran conjugated with fluorescein isothiocyanate, and then photographing while using an image intensifier (× 50 000). The experimental procedures were: (a) raising the temperature of an area of mesentery (0·33 × 0·21 inch) to 56 °C for 45 s; (b) infusing 10 ml of 0·9 per cent NaCl at a temperature of 55 °C into a mesenteric artery supplying the region being observed and then allowing the dog's own blood to perfuse this area; and (c) applying 2 ml of a 0·9 mg/ml solution of histamine in Ringer's solution topically to the mesentery; the histamine was washed off the mesentery 2 min later. The infusion of fluorescein-tagged materials was performed at about 10 min after completing an experimental procedure and still or cine film was exposed at 5, 10 and 60 s after infusion of the tagged materials.

The principal findings were that albumin and both the 70 000 and 150 000 MW dextrans passed from the circulating blood into the interstitial spaces primarily at bifurcations of venules when the tissue had not been exposed to heat or histamine. Following exposure to radiant heat, heated saline or histamine, venules and venous capillaries appeared to become more permeable to albumin and the two dextrans throughout their entire lengths. Venules and venous capillaries were less permeable to the 150 000 MW dextran than to albumin and the 70 000 MW dextran. No exit of tagged materials was observed from true capillaries.

Based upon these and other observations in this laboratory, the cause of increased permeability appears to be a swelling of endothelial cells which we believe results from imbibition of water when the cells are subjected to heat injury or to an abnormal concentration of histamine. Since cell membranes are relatively non-distensible, a swollen endothelial cell becomes more spherical (less hexahedron-shaped) and consequently its contacting surfaces tend to pull away from adjacent surfaces of other endothelial cells. This causes spaces to open between the cells permitting leakage of relatively large molecules through walls of venules and venous capillaries.