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 endoto xin shock, we compared its effects with those of endotoxin. We measure d arterial pressure (MAP), heart rate (HR), cardiac output (CO; thermo dilution), arterial lactate (C(a)lact), organ blood flow (radioactive microspheres), and organ vascular resistance in four groups of anesthe tized (pentobarbital) male Wistar rats (n = 7 per group), infused from t = 0 to t = 60 min with saline (group C: time matched control), endo toxin Escherichia coli O127:B8, 8 mg . kg(-1) (group E), a ''low PAF d ose'' (1 mu g . kg(-1)) to cause the same decrease in MAP as in group E (group PL), or a ''high PAF dose'' (3 mu g . kg(-1)) to cause the sa me decrease in CO as in group E (group PH). At t = 60 min, MAP had dec reased by 33% in E and PL, and by 55% in PH group. CO had decreased by 41% in the E and PH group. C(a)lact had increased in the E and PH gro up by 300 and 200%, respectively. In the 8, PL and PH group, coronary vascular resistance decreased. In the splanchnic organs, endotoxin cau sed a decrease in blood flow due to vasoconstriction, whereas PAF (bot h concentrations) caused vasodilation (except for spleen). Penal vascu lar resistance decreased (P < 0.05) in the PL group. In all groups, va scular resistance had increased (P < 0.05) in skin, and not changed in skeletal muscle (P < 0.05). Thus, hemodynamic changes after PAF infus ion were partially similar to those after endotoxin infusion (coronary vasodilation and vasoconstriction in spleen and skin). However, in th e splanchnic region (except the spleen) and in the kidney, PAF had a v asodilatory effect, whereas endotoxin had not. In separate experiments , PAF was not detectable in the blood of endotoxin-treated rats, where as it was in the PAF-treated rats. Additionally, the PAF antagonist BN 52021 had no beneficial effect on MAP, CO, and C(a)lact in rats treate d with endotoxin as a bolus. In conclusion, most systemic and regional hemodynamic changes during endotoxin shock are not mediated by PAF. ( C) 1993 Wiley-Liss, Inc.