title: Left ventricular dysfunction and acute lung injury induced by continuous administration of endotoxin in sheep.
abstract: 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)
authors.affiliation: Department of Anesthesiology, University of Texas Medical Branch, Galveston 77550, USA.
authors.forename: H
authors.initials: H
authors.lastname: Noda
authors.forename: S
authors.initials: S
authors.lastname: Noshima
authors.forename: H
authors.initials: H
authors.lastname: Nakazawa
authors.forename: J
authors.initials: J
authors.lastname: Meyer
authors.forename: D N
authors.initials: DN
authors.lastname: Herndon
authors.forename: H
authors.initials: H
authors.lastname: Redl
authors.forename: J
authors.initials: J
authors.lastname: Flynn
authors.forename: L D
authors.initials: LD
authors.lastname: Traber
authors.forename: D L
authors.initials: DL
authors.lastname: Traber
mesh_terms: 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
chemical_list: D004731:Endotoxins; D014409:Tumor Necrosis Factor-alpha; D013929:Thromboxane B2