Commercial albumin solution enhances endotoxin-induced vasoplegia and inflammation

The Gram-negative bacterium Escherichia coli, commonly involved in severe sepsis and septic shock, shed endotoxin that upon detection by the host triggers an inflammatory cascade. Efficiency of albumin solutions to restore hypovolemia during sepsis has been debated. To aid identification of subgroups of sepsis patients that may respond positively or negatively to treatment with albumin we investigated if preparations of albumin for medical use could affect endotoxin-induced inflammatory response.

Isolated human omental arteries obtained during surgery were incubated with endotoxin in the presence or absence of albumin solution. Isolated human monocytes were incubated with endotoxin in the presence or absence of five different commercially available albumin solutions. Vascular contractile response to noradrenaline and release of interleukin (IL)-1β, IL-6, IL-8, IL-10, and tumor necrosis factor (TNF)-α were measured.

Incubation with albumin together with endotoxin decreased median maximum contraction and increased release of IL-6 and IL-8 from the arteries compared to incubation with endotoxin alone. All albumin solutions except one significantly increased endotoxin-induced TNF-α release from monocytes. IL-6 and IL-10 were also increased and no concentration dependency of TNF-α release was observed above 2 mg mL^-1 . Incubation with albumin alone did not affect contraction or release of cytokines while no potentially endotoxin-enhancing contaminant could be identified.

We have shown that albumin solution in combination with endotoxin cause vasoplegia in human omental arteries, paralleled by an inflammatory response. This finding could explain the variable efficiency of albumin solutions for sepsis treatment.