Endothelial barrier resistance in multiple organs after septic and nonseptic challenges in the rat.

Local variations in endothelial permeability, hypothesized to play a role in the development of multiple-organ injury, were measured by 125I-labeled human serum albumin flux and leakage index in rats with a variety of challenges. The albumin flux significantly increased in the peritoneum, pancreas, stomach, and liver in acute pancreatitis; in the peritoneum and liver in abdominal sepsis; in the spleen, proximal small intestine, colon, liver, lungs, heart, and muscle in bacteremia; in the kidneys, liver, lungs, heart, brain, and muscle in endotoxemia; and in the peritoneum, proximal small intestine, colon, kidneys, liver, and heart after bradykinin administration. A redistribution of the tissue blood content, measured by 51Cr-labeled red blood cells, was noted. An increased albumin leakage index, assaying endothelial permeability considering local hemodynamic alterations, was noted in various organs in the different experimental groups. Thus septic and nonseptic challenges induce endothelial barrier injury. The endothelial resistance appears to be organ and/or tissue dependent and associated with a redistribution of blood.