Cardiac contractility was studied in a clinically relevant conscious swine
model simulating human hemodynamics during endotoxemia. The slope of the en
dsystolic pressure-volume relationship [end-systolic elastance (E-ES)] was
used as a load-independent contractility index. Chronic instrumentation in
10 pigs included two pairs of endocardial ultrasonic crystals for measuring
internal major and minor a;sial dimensions of the left ventricle, a microm
anometer for left ventricular pressure measurement, and a thermodilution pu
lmonary artery catheter. After a 10-day recovery period, control measuremen
ts of cardiac hemodynamic function were obtained. The following week, Esche
richia coil endotoxin (10 mu g.kg(-1).h(-1)) was administered intravenously
for 24 h. E-ES increased 1 h after endotoxin infusion and decreased beyond
7 h. The later hemodynamic changes resembled human cardiovascular performa
nce during endotoxemia more closely than the changes during the acute phase
. E-ES decreased in the later phase. A similar biphasic response of E-ES ha
s been reported during a tumor necrosis factor-alpha (TNF) challenge. Even
though plasma TNF was highest at 1 h and declined thereafter in this study,
no consistent relationship between TNF and E-ES was identified, and TNF le
vels did not correlate directly with the changes in E-ES.