By antiapoptotic effects and the induction of the heat-shock response,
zinc is supposed to be a promising means of
therapy during
sepsis. As
zinc also stimulates the expression of proinflammatory
cytokines, its administration during the proinflammatory stage of
septic shock might have adverse effects. Therefore, this study analyzes the influence of
zinc during the acute phase of
endotoxemia. In a pig model of acute
endotoxemia, animals were divided into two groups: group I (n = 5) with saline treatment and group II (n = 5) with
zinc treatment in close succession to
lipopolysaccharide (LPS) (1.0 mu g/kg
Escherichia coli endotoxin WO 111:B4). Hemodynamic and pulmonary monitoring was followed by combined reflection photometry, pulse oxymetry, blood gas samples, and temperature measurement. Plasma concentrations of
tumor necrosis factor (
TNF)alpha and
interleukin (IL)-6 were analyzed by
enzyme-linked
immunosorbent assay (ELISA). Morphology included the weight of the lungs, the width of the alveolar septae, and the paracentral
necrosis rate of the liver. After LPS infusion, group II (
zinc) showed an impressive and significant deterioration of all pulmonary and most of the hemodynamical parameters compared to group I (saline). Levels of
TNFalpha and
IL-6 measured were significantly higher after
zinc treatment. In accordance, we found significant more morphologic damages in group II (
zinc). The almost simultaneous infusion of
zinc and LPS complementary induced proinflammatory effects with a deleterious outcome. The same potentials characterizing
zinc as a promising tool of prophylactic
therapy in
sepsis seem to ban its use during the acute phase.