Left ventricular performance during continuous endotoxin-induced hyperdynamic endotoxemia in sheep

Cardiac function was studied in an unanesthetized ovine model of hyperdynamic endotoxemia. Sixteen sheep were instrumented with ultrasonic crystals on the left ventricle to measure changes in its external diameter, a pressure transducer in the left ventricle, and aortic and Swan-Ganz catheters. The animals received either Escherichia coli endotoxin [lipopolysaccharide (LPS), 10 ng · kg^-1 · min^-1; LPS group, n = 10] or an equivalent amount of 0.9% NaCl (sham group, n = 6). Between 1 and 8 h after LPS, a hypodynamic state with low cardiac output ensued (LPS 5.0 ± 0.2 vs. sham 6.3 ± 0.4 l · min^-1 · m^-2). During this period, the end- systolic pressure-diameter relationship, a sensitive index of myocardial contractility, was reduced (LPS 10.4 ± 1.2 vs. sham 17.2 ± 0.8 mmHg/mm). After this first phase, the sheep developed a persistent hyperdynamic state characterized by a significant increase in cardiac output. By 24 h after LPS administration, the cardiac output was 10.1 ± 0.5 l · min^-1 · m^-2 (sham 6.3 ± 0.3). Despite the marked elevation of cardiac output, the end- systolic pressure-diameter relationship had fallen to 8.5 ± 0.9 mmHg/mm (sham 16.0 ± 1.2). In a model of hyperdynamic state, an increased cardiac output occurs despite a significant depression in myocardial contractility.