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The induction of epinephrine shock by the intravenous infusion of epinephrine (10μg/kg/min) was characterized by an inability to maintain the initial stationary level of plasma epinephrine, leading to a progressive rise of epinephrine level up to a very high values (300-400μg/l) within a few hours. When epinephrine was infused intra-portally at the same rate, the arterial plasma ne attained a far lower initial level and neither a secondary rise nor urred during the infusion period of 4 hours. Thus the secondary lasma epinephrine level indicating the limit of epinephrine removal te of the intravenous infusion was found to be due to circumstances inish participation of the potential ability of the liver in removing le. The well documented reduction of splanchnic blood flow with a ogic dose of epinephrine has been suggested as the cause. The rise in plasma epinephrine level and the attendant shock were not with intravenous infusion at rates less than 5μg/kg/min during a usion period.Administration of glucocorticoid markedly potentiated the epinephrine removing capacity of the liver, while adrenalectomy reduced it. This might provide a satisfactory basis for the interpretation of the protective effect of glucocorticoid against epinephrine shock.

EPINEPHRINE SHOCK, ITS RELATION TO PLASMA EPINEPHRINE LEVEL AND THE MECHANISM OF ITS PROTECTION BY GLUCOCORTICOID