Acute endotoxemia increases left ventricular contractility and diastolic stiffness in calves.

We investigated the acute effects of endotoxemia on left ventricular (LV) contractility, relaxation, diastolic properties, and mechanical energetics in closed-chest calves. Twelve male calves (4 to 10 days old) were anesthetized with alpha-chloralose and instrumented to measure the LV pressure-volume relationship. Calves (n = 6) in the control group remained hemodynamically stable for 4 h. Calves (n = 6) administered endotoxin (0.1 microg/kg, O55:B5, i.v., over 0.5 h) had increased heart rate, mean pulmonary artery pressure, LV contractility (end-systolic elastance), chamber stiffness, and mechanical efficiency, no change in LV relaxation, and decreased mean systemic arterial pressure, cardiac output, and LV stroke work and pressure-volume area. Endotoxin-induced changes were maximal at t = 0.5 h, after which time all hemodynamic variables gradually returned towards baseline values. Intravenous administration of isoproterenol (0.02 microg x kg(-1) x min(-1)) alone or combined with phenylephrine (5 microg x kg(-1) x min(-1)) at t = 4 h produced similar increases in heart rate, end-systolic elastance, and cardiac output in control and endotoxin-treated groups. Our findings indicate that circulatory dysfunction, rather than LV dysfunction, predominates during acute endotoxemia (4 h) in chloralose-anesthetized, closed-chest neonatal calves.