Left ventricular dysfunction and acute lung injury induced by continuous administration of endotoxin in sheep.

H. Noda, S. Noshima, H. Nakazawa, J. Meyer, David Herndon, H. Redl, J. Flynn, L. D. Traber, D. L. Traber

Research output: Contribution to journalArticle

17 Citations (Scopus)

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)

Original languageEnglish (US)
Pages (from-to)291-298
Number of pages8
JournalShock (Augusta, Ga.)
Volume1
Issue number4
StatePublished - Apr 1994

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Acute Lung Injury
Left Ventricular Dysfunction
Endotoxins
Lipopolysaccharides
Sheep
Blood Pressure
Vascular Resistance
Arterial Pressure
Lung
Thromboxane B2
Pulmonary Hypertension
Tumor Necrosis Factor-alpha

ASJC Scopus subject areas

  • Physiology
  • Critical Care and Intensive Care Medicine

Cite this

Noda, H., Noshima, S., Nakazawa, H., Meyer, J., Herndon, D., Redl, H., ... Traber, D. L. (1994). Left ventricular dysfunction and acute lung injury induced by continuous administration of endotoxin in sheep. Shock (Augusta, Ga.), 1(4), 291-298.

Left ventricular dysfunction and acute lung injury induced by continuous administration of endotoxin in sheep. / Noda, H.; Noshima, S.; Nakazawa, H.; Meyer, J.; Herndon, David; Redl, H.; Flynn, J.; Traber, L. D.; Traber, D. L.

In: Shock (Augusta, Ga.), Vol. 1, No. 4, 04.1994, p. 291-298.

Research output: Contribution to journalArticle

Noda, H, Noshima, S, Nakazawa, H, Meyer, J, Herndon, D, Redl, H, Flynn, J, Traber, LD & Traber, DL 1994, 'Left ventricular dysfunction and acute lung injury induced by continuous administration of endotoxin in sheep.', Shock (Augusta, Ga.), vol. 1, no. 4, pp. 291-298.
Noda H, Noshima S, Nakazawa H, Meyer J, Herndon D, Redl H et al. Left ventricular dysfunction and acute lung injury induced by continuous administration of endotoxin in sheep. Shock (Augusta, Ga.). 1994 Apr;1(4):291-298.
Noda, H. ; Noshima, S. ; Nakazawa, H. ; Meyer, J. ; Herndon, David ; Redl, H. ; Flynn, J. ; Traber, L. D. ; Traber, D. L. / Left ventricular dysfunction and acute lung injury induced by continuous administration of endotoxin in sheep. In: Shock (Augusta, Ga.). 1994 ; Vol. 1, No. 4. pp. 291-298.
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AU - Noshima, S.

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AU - Herndon, David

AU - Redl, H.

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AB - 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)

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