Infusion of ultrafiltrate from endotoxemic pigs depresses myocardial performance in normal pigs

We previously showed a beneficial effect of hemofiltration on hemodynamics of endotoxic shock pigs. To test the hypothesis that this effect of hemofiltration is caused by convective removal of factors that adversely effect hemodynamics during endotoxemia, we infused ultrafiltrate from endotoxic shock pigs into healthy pigs. Their hemodynamics were compared with those of pigs who were infused with ultrafiltrate from healthy pigs. Twelve anesthetized and ventilated pigs were hemodynamically monitored for 150 minutes following the infusion of 2 L of ultrafiltrate from 12 donor pigs. The acceptor pigs were randomly divided into two groups; group 1 received ultrafiltrate from pigs who were hemofiltered after the infusion of 0.5 mg/kg endotoxin over 30 minutes; group 2 served as a control group, receiving ultrafiltrate from healthy donor pigs. Group 1 showed a decrease in mean arterial pressure of 28 ± 7 mm Hg (mean ± SEM) versus an increase of 17 ± 3 mm Hg in group 2 ( P < .04). Mean pulmonary artery pressure increased more in group 1 than in group 2 (9 ± 2 mm Hg versus 1 ± 1 mm Hg, P < .04). The decrease in cardiac output in group 1 was greater than in group 2 (3.3 ± 0.2 L/ min v 0.3 ± 0.3 L /min, P < .02) and was due to a decrease in stroke volume. The decrease in right ventricular ejection fraction was also greater (0.15 ± 0.02 v 0.01 ± 0.00, P < .01). Systemic vascular resistance, right atrial pressure, right ventricular end-diastolic volume, pulmonary wedge pressure and heart rate did not differ between groups. In contrast to ultrafiltrate from healthy pigs, ultrafiltrate from endotoxic shock pigs contains soluble, filtrable factors that increase pulmonary artery pressure and depress cardiac performance.