• A Ricard-Hibon, M R Losser, R Kong, S Beloucif, B Teisseire, and D Payen.
• Département d'Anesthésie-Réanimation, Centre Hospitalier Universitaire Lariboisière, Assistance Publique-Hôpitaux de Paris, France.
• Intensive Care Med. 1998 Sep 1; 24 (9): 959966959-66.

ObjectiveThis study aimed to evaluate the impact of fluid loading on hemodynamics and vascular hypocontractility to norepinephrine (NE) in an endotoxic shock model.DesignMean arterial pressure (MAP), aortic blood flow velocity (AoV, 20 MHz Doppler) and aortic conductance (AoC = AoV/MAP) were studied during 180 min (T0-T180) in 41 anesthetized and ventilated rabbits.InterventionsShock was induced by a 600 micrograms/kg bolus injection of endotoxin. Fluid loading (20 ml/kg colloids) was infused from T90 to T120. Dose-response curves to NE were performed at T0, T60 and T120 in endotoxic and non-endotoxic animals with or without fluid loading.Measurements And ResultsEndotoxin decreased pressure (-23%, p < 0.05) and flow (-42%, p < 0.05) corresponding to a decrease in conductance (-19%, p < 0.05). Fluid loading did not improve hypotension but markedly increased systemic flow (+51%, p < 0.01), corresponding to a hyperkinetic syndrome. Vascular reactivity to NE was impaired after endotoxin at T60 since the pressure response to NE was depressed (p < 0.01) and flow did not decrease. In non-fluid-loaded groups, the pressure response to NE recovered at T120, with no reduction in flow. In fluid-loaded endotoxic animals, however, the pressure response to NE was still impaired at T120 (p < 0.05), but with a decrease in flow.ConclusionsFluid loading transformed the hypodynamic profile of endotoxic shock into a hyperdynamic state without improving blood pressure. Depressed vascular reactivity to NE was observed in both hyperdynamic and hypodynamic states, suggesting that a reduced vascular reactivity does not necessarily imply systemic vasodilation.

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