Sepsis remains the most common cause of death in intensive care units of the developed world. Accurate models of this disease syndrome are crucial for to the understanding of the complex pathophysiology of this disorder. The administration of a small dose of lipopolysaccharide to healthy volunteers is one such model of spontaneous human sepsis. Although this human endotoxemia model appears to be reasonably effective in mimicking early biochemical, metabolic, hematologic and cardiovascular septic responses in septic shock, the ability to mimic other aspects of human sepsis is open to question. The current study demonstrates that human experimental endotoxemia fails to generate evidence of increased vascular permeability within the relatively short time frame of the study.