Abstract
A remarkable number of clinical trials have been performed in the past decade to evaluate drugs for the treatment of sepsis. The mechanism of action of most of these agents is based on one of two unproved assumptions relating to sepsis in humans. The first is that endotoxin (bacterial lipopolysaccharide) contributes to the morbidity and mortality caused by infection with gram-negative bacteria. The second assumption is that a major part of the pathophysiology in patients with sepsis is due to an overproduction of one or many secondarily induced host mediators. The evidence for these widespread beliefs is that when lipopolysaccharide . . .