To evaluate the role of platelet activating factor (PAF) during endotoxin shock, we compared its effects with those of endotoxin. We measured arterial pressure (MAP), heart rate (HR), cardiac output (CO; thermodilution), arterial lactate (Calact), organ blood flow (radioactive microspheres), and organ vascular resistance in four groups of anesthetized (pentobarbital) male Wistar rats (n = 7 per group), infused from t = 0 to t = 60 min with saline (group C: time matched control), endotoxin Escherichia coli O127:B8, 8 mg.kg-1 (group E), a "low PAF dose" (1 microgram.kg-1) to cause the same decrease in MAP as in group E (group PL), or a "high PAF dose" (3 micrograms.kg-1) to cause the same decrease in CO as in group E (group PH). At t = 60 min, MAP had decreased by 33% in E and PL, and by 55% in PH group. CO had decreased by 41% in the E and PH group. Calact had increased in the E and PH group by 300 and 200%, respectively. In the E, PL and PH group, coronary vascular resistance decreased. In the splanchnic organs, endotoxin caused a decrease in blood flow due to vasoconstriction, whereas PAF (both concentrations) caused vasodilation (except for spleen). Renal vascular resistance decreased (P < 0.05) in the PL group. In all groups, vascular resistance had increased (P < 0.05) in skin, and not changed in skeletal muscle (P < 0.05). Thus, hemodynamic changes after PAF infusion were partially similar to those after endotoxin infusion (coronary vasodilation and vasoconstriction in spleen and skin).(ABSTRACT TRUNCATED AT 250 WORDS)