Systemic and regional hemodynamic changes during endotoxin or platelet activating factor (PAF)-induced shock in rats.

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)