Left ventricular dysfunction and acute lung injury induced by continuous administration of endotoxin in sheep.
Sixteen sheep were surgically prepared for chronic study. Seven days later, Escherichia coli endotoxin (10 ng/kg/min, lipopolysaccharide (LPS) group, n = 10) or an equivalent amount of 0.9% NaCl (Control group n = 6) was administered. Between 1 and 8 h post-LPS, there was a hypodynamic state with low cardiac index (CI, LPS 5.0 +/- 0.2; sham 6.3 +/- 0.4 liters/min/m2 at 4 h). During this period, the left ventricular end-systolic pressure-diameter relationship (ESPDR), a sensitive index of myocardial contractility, was also lower (LPS 10.4 +/- 1.2; sham 17.2 +/- 0.8 mmHg/mm). Mean pulmonary arterial pressure (PAP) and pulmonary vascular resistance index (PVRI) were remarkably increased 1 h after the administration of LPS (PAP:LPS 37.5 +/- 1.9; sham 21.8 +/- 0.9 mmHg, PVRI: LPS 600 +/- 58; sham 158 +/- 23 dynes x s x cm-5 x m2). The early changes in cardiopulmonary function occurred concomitantly with an elevation in tumor necrosis factor (LPS 1221 +/- 520; sham 0 +/- 0 pg/ml) and thromboxane B2 (LPS 1382 +/- 266; baseline 82 +/- 20 pg/ml) in arterial blood. Following this first phase, the sheep presented a persistent hyperdynamic state characterized by a significant increase in CI. The ESPDR continued to fall. By 24 h post-LPS the CI was 10.1 +/- 0.5 liters/min/m2 (sham, 6.3 +/- 0.3) but the ESPDR had fallen to 8.2 +/- 2.3 mmHg/mm (sham 16.0 +/- 3.0). The pulmonary hypertension was maintained for the duration of the LPS infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Noda
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Department of Anesthesiology, University of Texas Medical Branch, Galveston 77550, USA.
Noshima
S
S
Nakazawa
H
H
Meyer
J
J
Herndon
D N
DN
Redl
H
H
Flynn
J
J
Traber
L D
LD
Traber
D L
DL
D000208:Acute Disease; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002302:Cardiac Output / Q000187:drug effects / Q000502:physiology; D004731:Endotoxins / Q000008:administration & dosage / Q000633:toxicity*; D005260:Female; D006331:Heart Diseases / Q000209:etiology* / Q000503:physiopathology; D008168:Lung / Q000187:drug effects* / Q000503:physiopathology; D055370:Lung Injury; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D009504:Neutrophils / Q000187:drug effects; D011652:Pulmonary Circulation / Q000187:drug effects / Q000502:physiology; D012756:Sheep; D013929:Thromboxane B2 / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology; D016277:Ventricular Function, Left / Q000187:drug effects* / Q000502:physiology
D004731:Endotoxins; D014409:Tumor Necrosis Factor-alpha; D013929:Thromboxane B2