J. Hung et Wyw. Lew, TEMPORAL SEQUENCE OF ENDOTOXIN-INDUCED SYSTOLIC AND DIASTOLIC MYOCARDIAL DEPRESSION IN RABBITS, The American journal of physiology, 265(3), 1993, pp. 80000810-80000819
Twelve anesthetized rabbits received endotoxin (175 +/- 38 mug/kg iv,
mean +/- SD) to evaluate the temporal sequence of alterations in left
ventricular (LV) function. LV volume was calculated from LV minor- and
long-axis diameters, and wall thickness was measured with sonomicrome
ters. Hypotension, acidosis, and hypoxia were immediately corrected to
eliminate these causes of myocardial depression. LV dilation develope
d early (1.2 +/- 0.5 h) with a significant (21 +/- 23%) increase in en
d-diastolic volume measured at a LV end-diastolic pressure of 5 +/- 6
mmHg. The LV stiffness did not change, and the LV dilation did not pro
gressively worsen. Significant systolic depression developed later (2.
8 +/- 1.0 h) with a 32 +/- 22% increase in end-systolic volume measure
d at a LV end-systolic pressure of 69 +/- 9 mmHg. The late preterminal
phase (4.1 +/- 0.8 h) was characterized by a progressive increase in
end-systolic volume (73 +/- 41% above control) and a significant (53 /- 34%) increase in tau, the time constant of LV pressure fall. Diasto
lic abnormalities (LV dilation and increased tau) were not attributabl
e to depressed contractility or altered hemodynamics. We conclude that
endotoxin impairs systolic and diastolic LV function with distinct di
fferences in time course. This suggests that contractility, relaxation
, and passive LV properties are impaired by different endotoxin-mediat
ed pathways and/or have different sensitivities to endotoxin.