Oxygen extraction is altered by endotoxin during tamponade-induced stagnant hypoxia in the dog.

The present study used a model of cardiac tamponade to investigate the effects of endotoxin on the oxygen extraction capabilities of the body during an acute reduction in blood flow, when blood volume and arterial oxygen content were maintained. In 21 pentobarbital anesthetized, mechanically ventilated dogs, two catheters were introduced into the pericardial space to induce cardiac tamponade, and simultaneously to measure the intrapericardial pressure. Oxygen uptake (VO2) was determined from the expired gases. Oxygen delivery (DO2) was calculated by the product of the thermodilution cardiac index and the arterial oxygen content. Eleven dogs received 2 mg/kg Escherichia coli endotoxin, followed by generous saline infusion (20 ml/kg.hr). Ten dogs served as a control group. In each dog, DO2 was progressively reduced by pericardial saline infusion at a rate of 40 ml/hr for the first hour and 30 ml/hr thereafter. Critical O2 delivery (DO2crit) and critical O2 extraction ratio (O2ERcrit) were determined from a plot of VO2/DO2 for each individual dog. The DO2crit was greater in the endotoxic than in the control group (12.1 +/- 3.1 ml/kg.min vs. 9.6 +/- 1.6 ml/kg.min; P < 0.05). Endotoxin at the dose used did not alter VO2 (or critical VO2). Accordingly, O2ERcrit was significantly lower in the endotoxic than in the control animals (47.2% +/- 5.7% vs. 60.3% +/- 10.6%; P < 0.01). The mixed venous PO2 levels at DO2crit were higher in the endotoxic than in the control group (30.6 +/- 6.1 mm Hg vs. 25.4 +/- 5.2 mm Hg; P < 0.05). Arterial blood lactate concentration was higher in the endotoxic than in the control dogs.(ABSTRACT TRUNCATED AT 250 WORDS)