Cardiac contractility is not depressed in early canine endotoxic shock.

We investigated effects of acute endotoxemia (Escherichia coli endotoxin, 1 mg/kg, intravenously) on left ventricular (LV) function in the first 4 h after induction of endotoxic shock in anesthetized canine preparations (n = 7 each, endotoxin and control groups). LV pressure and conductance (volume) catheters were used to construct pressure-volume loops. Transient inferior vena cava occlusion was used to rapidly and reversibly alter LV end-diastolic volume. LV contractility was assessed from the slope of the LV end-systolic pressure-volume relationship (Ees) and from preload-recruitable stroke work (PRSW), and from their change (DeltaEes and DeltaPRSW, respectively, measured at 2 and 4 h only), in response to a dobutamine infusion (5 microg/kg/min). Diastolic function and arterial tone were assessed as the maximal negative change in filling pressure versus time (max -dP/dt), filling rate, and arterial elastance (Ea), respectively. Ees, PRSW, Ea, diastolic function, and hemodynamics were measured hourly. Endotoxemia induced an immediate hypotensive, hyperdynamic, tachycardic state with progressive lactic acidosis. By 2.5 h after endotoxin infusion, heart rate returned to preendotoxin and control levels, but the other changes remained. However, no change occurred in LV Ees, DeltaEes, PRSW, DeltaPRSW, diastolic function, or Ea during the 4-h measurement interval. The cardiovascular collapse seen during the first 4 h of endotoxemia is therefore not due even partly to alterations in LV contractility.