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1 We investigated hepatic blood¯ow, O 2 exchange and metabolism in porcine endotoxic shock (Control, n=8; Endotoxin, n=10) with administration of hydroxyethylstarch to maintain arterial pressure (MAP)460 mmHg. 2 Before and 12, 18 and 24 h after starting continuous i.v. endotoxin we measured portal venous and hepatic arterial blood¯ow, intracapillary haemoglobin O 2 saturation (Hb-O 2 %) of the liver surface and arterial, portal and hepatic venous lactate, pyruvate, glyercol and alanine concentrations. Glucose production rate was derived from the plasma isotope enrichment during infusion of [6, H 2 ]-glucose. 3 Despite a sustained 50% increase in cardiac output endotoxin caused a progressive, signi®cant fall in MAP. Liver blood¯ow signi®cantly increased, but endotoxin aected neither hepatic O 2 delivery and uptake nor mean intracapillary Hb-O 2 % and Hb-O 2 % frequency distributions. 4 Endotoxin nearly doubled endogenous glucose production rate while hepatic lactate, alanine and glycerol uptake rates progressively decreased signi®cantly. The lactate uptake rate even became negative (P50.05 vs Control). Endotoxin caused portal and hepatic venous pH to fall signi®cantly concomitant with signi®cantly increased arterial, portal and hepatic venous lactate/pyruvate ratios. 5 During endotoxic shock increased cardiac output achieved by colloid infusion maintained elevated liver blood¯ow and thereby macro-and microcirculatory O 2 supply. Glucose production rate nearly doubled with complete dissociation of hepatic uptake of glucogenic precursors and glucose release. Despite well-preserved capillary oxygenation increased lactate/pyruvate ratios re¯ecting impaired cytosolic redox state suggested deranged liver energy balance, possibly due to the O 2 requirements of gluconeogenesis.

Fat emulsions containing medium chain triglycerides (MCT) have recently been introduced into clinical practice as a component of total parenteral nutrition. Since several authors reported increased pulmonary artery pressure and impaired gas exchange during intravenous (i.v.) fat use, in particular in septic patients, we studied the pulmonary hemodynamic and gas exchange effects of i.v. fat containing MCT and long chain triglycerides (LCT) in patients with sepsis syndrome. As the effects of fat emulsions have been attributed to increased formation of prostanoids, the production of thromboxane A2 and prostacyclin was investigated by the determination of urinary thromboxane B2 and 6-keto-prostaglandin F2 alpha, respectively. The i.v. fat use did not induce any alterations in pulmonary hemodynamics and gas exchange, the distribution of ventilation and perfusion nor urinary prostaglandin content. We conclude that fat emulsions containing MCT induce little alterations in pulmonary hemodynamics and gas exchange. This result is probably due to reduced prostaglandin formation because fat emulsions containing MCT provide less prostaglandin precursors than pure LCT emulsions.