Objective:To assess the effects of continuous venovenous hemofiltration (CVVH) on global and regional hemodynamics, plasma lactate, and tumor necrosis factor-α (TNF-α) levels during endotoxic shock in dogs.Methods:Thirty pentobarbital-anesthetized and mechanically ventilated dogs were divided into six groups of five dogs each. Group 1 served as a control, undergoing CVVH at 3 L/hr without endotoxin. Group 2 served as the endotoxin-alone time-matching group. Group 3 received CVVH 1 hr after endotoxin at 3 L/hr for 270 mins. Group 4 received CVVH 1 hr after endotoxin at 3 L/hr for 150 mins and at 6 L/hr for an additional 120 mins. Group 5 and group 6 received the ultrafiltrate from group 1 and group 3, respectively.Measurements and Main Results:Three hours after endotoxin challenge, dogs treated with CVVH at 3 L/hr had a higher cardiac output (4.9 ± 0.6 vs. 2.9 ± 0.6 L/min;p< .05) and stroke volume (35 ± 7 vs. 20 ± 4 mL;p< .05) and a lower pulmonary vascular resistance (116 ± 26 vs. 331 ± 126 dyne·sec/cm5;p< .05) than the endotoxin-alone group. Five hours after endotoxin, dogs treated with CVVH at 6 L/hr also had higher hepatic (464 ± 164 vs. 126 ± 75 mL/min;p< .05) and femoral (95 ± 46 vs. 30 ± 34 mL/min;p< .05) blood flow. Moreover, dogs treated with CVVH at 6 L/hr had higher mean arterial blood pressure (84 ± 24 vs. 40 ± 15 mm Hg;p< .05) and left ventricular stroke work index (1.1 ± 0.6 vs. 0.2 ± 0.2 g/kg;p< .05) than the endotoxin-alone group. Plasma lactate levels were lower in the CVVH group at 6 L/hr (2.7 ± 1.1 mmol/L) than in the endotoxin-alone group (4.4 ± 0.6 mmol/L;p< .05). Plasma TNF-α levels were unaffected, and only minor amounts of TNF-α were found in the ultrafiltrate.Conclusion:In this acute endotoxic shock model, CVVH at 3 L/hr improved cardiac performance and decreased pulmonary vasoconstriction. Moreover, CVVH at 6 L/hr also increased arterial blood pressure and left ventricular stroke work, increased hepatic and femoral arterial blood flow, and decreased blood lactate levels. These effects were not attributable to TNF-α removal.