ACUTE ENDOTOXEMIA INCREASES LEFT VENTRICULAR CONTRACTILITY AND DIASTOLIC STIFFNESS IN CALVES

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Abstract
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 α-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 ug/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 αg.kg-1.min-1) alone or combined with phenylephrine (5 αg.kg-1.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.

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