The effects of hydroxyethyl starch on lung capillary permeability in endotoxic rats and possible mechanisms

In this study we examined the effects of hydroxyethyl starch (HES 200/0.5) on lung capillary permeability in endotoxic rats and explored the possible mechanisms. Male Wistar rats were randomly divided into seven groups treated with saline, lipopolysaccharide (LPS; 6 mg/kg), LPS plus HES (3.75, 7.5, 15, or 30 mL/kg), or HES (30 mL/kg) alone for 4 or 2 h. Lung capillary permeability, lung neutrophil accumulation, expression of CD11b on the blood neutrophil cell surface, lung cytokine-induced neutrophil chemoattractant protein level, and nuclear factor kappa B (NF-kappaB) activation in blood neutrophils and lungs were measured. HES at doses of 3.75 and 7.5 mL/kg significantly reduced LPS-induced increases of lung capillary permeability. HES was found to inhibit lung neutrophil accumulation, cytokine-induced neutrophil chemoattractant protein, and NF-kappaB activation in parallel and to inhibit CD11b expression in a dose-dependent manner. These findings demonstrate that HES has beneficial effects on capillary leak in acute lung injury and that the mechanisms underlying this action involve an antiinflammatory effect of HES, including inhibition of NF-kappaB activation.

A randomized, controlled laboratory experiment indicated that hydroxyethyl starch (HES) could reduce increased lung capillary permeability in endotoxemia. This effect may be due to an antiinflammatory effect of HES.