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After induction of septic shock, the animals were randomized to sham operation (n = 9) or treatment with the dopamine-D2 receptor agonist (CLP = 6, LPS = 6). In another group of rats, septic shock was induced after stabilization of a controlled hemorrhagic-shock animal model (n = 6). Intravenous infusion of a dopamine-D2 receptor agonist (30 microg/kg per hour) started at the time of sepsis and was continued for 72 hours. In another group of rats, plasma catecholamines were administered (CLP or LPS = 6). In addition, catecholamines were infused in a hemorrhagic-shock animal model after stabilization (CLP = 4, LPS = 4). Organ function was assessed for 72 hours by measuring hemodynamics, survival, kidney function, and tissue water content. The dopamine-D2 receptor agonist enhanced the survival time of septic shock rats from 34% +/- 8% to 57% +/- 13% (P =.02) and prevented the onset of shock in hemorrhagic-shock animals. The dopamine-D2 receptor agonist had no effect on erythrocyte membrane sodium transport activity in septic or cardiogenic shock. Catecholamine infusion markedly increased erythrocyte sodium transport activity, and it was associated with a significantly decreased survival (P =.04). These results indicate that dopamine-D2 receptor stimulation prevents the onset of septic shock in the most severe model of this syndrome and fails to improve the outcome of septic shock. 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