Effects of propofol on hemodynamic and inflammatory responses to endotoxemia in rats

Objective: To document the effects of propofol on the hemodynamic and infla mmatory responses to endotoxemia in an animal model. Design: Randomized, prospective laboratory study. Setting: University experimental laboratory. Subjects: Thirty-two male rats. Interventions: The animals were randomly assigned to one of four groups: a) endotoxemia group (n = 8), which received intravenous Escherichia coil end otoxin (15 mg/kg over 2 mins); b) control group (n = 8), which was treated identically to the endotoxemia group except for the substitution of 0.9% sa line for endotoxin; c) propofol group (n = 8), which was treated identicall y to the control group but also received propofol (10 mg/kg bolus, followed by infusion at 10 mg/kg/hr) immediately after the injection of 0.9% saline ; and d) propofol-endotoxemia group (n = 8), which was treated identically to the endotoxemia group with the additional administration of propofol (10 mg/kg bolus, followed by infusion at 10 mg/kg/hr) immediately after endoto xin injection, Measurements and Main Results: Hemodynamics, arterial blood gases, and acid -base status were recorded and the blood propofol concentrations and plasma cytokine concentrations were measured during the 5-hr observation. Microsc opic findings of lung tissue for each group were obtained at necropsy, The systolic arterial pressure and heart rate of the propofol-endotoxemia group were similar to those of the endotoxemia group, The increases in the plasm a cytokine (tumor necrosis factor, interleukin-6, and interleukin-10) conce ntrations, in the base deficit, and in the infiltration of neutrophils in t he air space or vessel walls of the lungs were attenuated in the propofol-e ndotoxemia group compared with the endotoxemia group. Conclusions: Propofol attenuated cytokine responses, base deficit, and acti vation of neutrophils to endotoxemia. These findings suggest that propofol may inhibit inflammatory response and prevent the development of metabolic acidosis during endotoxemia.