Effects of serum and endotoxin in experimental lung injury

Lipopolysaccharide (LPS) is in large part responsible for the lung injury that occurs in the sepsis syndrome. Recent work has shown the ability of LPS alone to induce injury in endothelial monolayers, though the LPS effect is enhanced in the presence of serum. We previously demonstrated that low-dose LPS (50 ng/mL) can lead to lung injury in an isolated perfused rabbit lung model. To examine the effect of serum on LPS-induced injury rabbit lungs were perfused with increasing doses of rabbit serum in the presence and absence of LPS. There was no increase in total weight gained by the lung,Qf, with either 5% serum, 10% serum, or 10% serum with LPS. However vascular permeability as measured by hydraulic conductance was increased with increasing doses of serum. This effect was not enhanced by the addition of LPS. These results provide evidence that serum alone may cause lung injury, perhaps through the activation of complement or other mediators.