AIM To investigate the action mechanism of
dexamethasone in treating
endotoxic shock. METHODS 24 rabbits were injected
iv endotoxin 600 μg·kg -1 to induce
endotoxic shock. 30 min later, they were injected iv normal saline (control group), or dexamethasone (Dex) 2 mg·kg -1 , inhibitor of NO synthetase N G Methyl L Arginine ( L NMA) 10 mg·kg -1 , and inhibitor of endothelin converting enzyme phosphoramidon (Phos) 2 mg·kg -1 respectively. The hemodynamic index, plasma nitrate and ET 1 concentrations were measured at regular intervals. RESULTS The results showed that the plasma nitrate and ET 1 concentrations increased obviously, while the
hemodynamics progressively deteriorated after endotoxin injection in rabbits. L NMA and Phos inhibited the increases of nitrate or ET 1 respectively, and reduced their baseline levels. The hemodynamics in L NMA and Phos groups were just transiently improved, not soon deteriorated and become indifferent from control group. Dex inhibited the excessive increases of nitrate and ET 1 while did not affect their baseline levels. The hemodynamics was the most steady in Dex group. CONCLUSIONS These data suggested that the antagonism of Dex against the increases of plasma NO and ET 1 during endotoxic shock may be one of the important action mechanism of its anti endotoxic shock.