Model for environmental heat damage of the blood vessel barrier

Environmental heat stress may result in loss of fluid from the vascular space, which can lead to circulatory shock. Since the endothelium serves as the blood vessel barrier between the vascular and interstitial spaces, direct heat damage to this tissue may contribute to such fluid loss. This study modeled heat influences on the actin cytoskeletal proteins that provide the tensile forces that sustain endothelial junctional integrity or barrier function. Heat effects on bovine aortic endothelial cell (BAEC) F-actin and F-actin stress fibers (FASFs) were correlated with intercellular permeability (IP). F-actin concentration and FASF distribution were analyzed by quantitation of the specific binding of rhodamine phalloidin (RP) to F-actin and by observing the fluorescence of RP-FASF complexes, respectively. Dextran fluorescein IP was determined. The IP was elevated (p < 0.05) at 43 degrees C, but not at 41 degrees C. At 43 degrees C, BAECs were rounded and had disrupted FASFs and diminished cell-to-cell apposition. Similar cells were seen at 41 degrees C, but these were interspersed among FASF-containing cells to sustain apposition. Thus, disruption of FASFs correlated with increases in IP. F-actin was increased (p < 0.05) after hyperthermia. Since G-actin is more susceptible to irreversible heat denaturation, F-actin sustainment may function to preserve the actin pool and prevent irrevocable loss of the blood vessel barrier after heat stress.