We studied the hepato-splanchnic vascular response and changes in O-2 extraction capabilities to a reduction in blood flow following endotoxemia. Fourteen anesthetized and mechanically ventilated dogs were divided into two groups of seven each. Group 1 received 2 mg/kg of E. coli endotoxin, and group 2 served as a control. After initial fluid resuscitation following endotoxic shock, regional blood flow estimated by an ultrasonic technique increased similarly in the hepatic artery, portal vein, and mesenteric artery, but microvascular blood flow estimated by a laser Doppler technique was lower in the liver than in the intestinal mucose. When blood flow was reduced by cardiac tamponade, endotoxin-treated animals had greater whole body and regional critical O-2 delivery (DO2crit) and lower whole body, liver, and intestinal critical O-2 extraction ratios (O2ERcrit). DO2crit was higher in the liver than in intestine but O2ERcrit was similar in the two organs. Whole body DO2crit at the onset of organ O-2 supply dependency was similar under control (9.4 +/- 1.9 mL/kg . min for whole body, 10.3 +/- 4.7 mL/kg . min for liver, and 10.0 +/- 2.6 mL/kg min for intestine) and endotoxic conditions (13.6 +/- 3.2 mL/kg min for whole body, 15.6 +/- 2.7 mL/kg min for liver, and 15.4 +/- 8.7 mL/kg . min for intestine). We conclude that fluid-resuscitated endotoxic shock in dogs is characterized by blood flow redistribution within the liver and intestine. Microvascular depression may be more severe in the liver than in the intestinal mucosa, although the whole body, the liver, and the intestine became O-2 supply-dependent simultaneously. (C) 1999 Academic Press.