Hyperdynamic sepsis in baboons: I. Aspects of hemodynamics

The baboon has a number of advantages as a shock model, as its physiological as well as its biochemical behaviour is similar to man. Therefore we have tried to set up a model to mimic the early hyperdynamic phase of clinical sepsis. Seven baboons, 21-25 kg body weight were kept under EEG servocontrolled anesthesia for 8 hr. During this time live E. coli (ATC #33985) 2 x 10(10) BW/8 hr were continuously infused intravenously. Adequate fluid supply with Ringer's solution (up to 40 ml/kg/hr) was given to keep the pulmonary artery wedge pressure at baseline levels; this procedure resulted in a hyperdynamic response with a cardiac output (CO) 20-35% above baseline and a decrease (20-39%) in mean arterial pressure (MAP), leading to a 50% decrease in peripheral resistance. The pulmonary vascular changes were reflected in an increase of the mean pulmonary pressure (PA) to 42% above baseline and a marked rise in pulmonary vascular resistance (PVR) to 50% above baseline with no additional changes in pulmonary gas exchange. After 8 hr both CO and MAP were inversely correlated (r = 0.9-1) with dramatically increased catecholamine plasma levels (15 times above baseline). With continuous infusion of live E. coli (blood levels 10(5)-10(6) CFU/ml) and massive fluid supply we have successfully mimicked hyperdynamic sepsis with severe organ failure after an 8-hr observation period.