Canine left ventricular performance during LD50 endotoxemia.

Previous reports of the effect of endotoxin shock on cardiac performance have not achieved uniform results. These discrepancies have possibly been caused by the use of indices of cardiac performance that may have been sensitive to altered heart rate or preconditions of cardiac contraction as well as altered cardiac performance. We tested the hypothesis that, following a median lethal dose (LD50) of E. coli endotoxin, cardiac performance would be diminished in nonsurviving animals and maintained in surviving animals. We elected to employ the analysis of the end-systolic pressure-diameter relationship (sigma ES) as well as other measurements of cardiac performance to test this hypothesis. We established that the sigma ES measurement was independent of increased and decreased afterload and relatively insensitive to altered heart rate. In the nonsurviving animals, sigma ES exhibited a marked depression following endotoxin a administration. In the surviving animals, sigma ES exhibited a nonsignificant decrease followed by a return toward preendotoxin values. All other cardiodynamic measurements were uninterpretable due to the marked changes in heart rate, peripheral vascular function, aortic pressure, and cardiac output. We conclude that, following endotoxin administration, those animals that exhibited a diminished myocardial contractility failed to survive more than 2.5 h postendotoxin, whereas the surviving animals were able to restore normal cardiac contractility. Thus survival of endotoxin administration is associated with the maintenance of normal cardiac contractility.