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  • An Ovine Model of Hyperdynamic Endotoxemia and Vital Organ Metabolism

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    Accepted Manuscript (AM)
    Author(s)
    Byrne, L
    Obonyo, NG
    Diab, S
    Dunster, K
    Passmore, M
    Boon, AC
    Hoe, LS
    Hay, K
    Van Haren, F
    Tung, JP
    Cullen, L
    Shekar, K
    Maitland, K
    Fraser, JF
    Griffith University Author(s)
    Fraser, John F.
    See Hoe, Louise
    Year published
    2018
    Metadata
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    Abstract
    Background: Animal models of endotoxemia are frequently used to understand the pathophysiology of sepsis and test new therapies. However, important differences exist between commonly used experimental models of endotoxemia and clinical sepsis. Animal models of endotoxemia frequently produce hypodynamic shock in contrast to clinical hyperdynamic shock. This difference may exaggerate the importance of hypoperfusion as a causative factor in organ dysfunction. This study sought to develop an ovine model of hyperdynamic endotoxemia and assess if there is evidence of impaired oxidative metabolism in the vital organs. Methods: ...
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    Background: Animal models of endotoxemia are frequently used to understand the pathophysiology of sepsis and test new therapies. However, important differences exist between commonly used experimental models of endotoxemia and clinical sepsis. Animal models of endotoxemia frequently produce hypodynamic shock in contrast to clinical hyperdynamic shock. This difference may exaggerate the importance of hypoperfusion as a causative factor in organ dysfunction. This study sought to develop an ovine model of hyperdynamic endotoxemia and assess if there is evidence of impaired oxidative metabolism in the vital organs. Methods: Eight sheep had microdialysis catheters implanted into the brain, heart, liver, kidney, and arterial circulation. Shock was induced with a 4 h escalating dose infusion of endotoxin. After 3 h vasopressor support was initiated with noradrenaline and vasopressin. Animals were monitored for 12 h after endotoxemia. Blood samples were recovered for hemoglobin, white blood cell count, creatinine, and proinflammatory cytokines (IL-1Beta, IL-6, and IL-8). Results: The endotoxin infusion was successful in producing distributive shock with the mean arterial pressure decreasing from 84.5 ± 12.8 mm Hg to 49 ± 8.03 mm Hg (P < 0.001). Cardiac index remained within the normal range decreasing from 3.33 ± 0.56 L/min/m2 to 2.89l ± 0.36 L/min/m2 (P = 0.0845). Lactate/pyruvate ratios were not significantly abnormal in the heart, brain, kidney, or arterial circulation. Liver microdialysis samples demonstrated persistently high lactate/pyruvate ratios (mean 37.9 ± 3.3). Conclusions: An escalating dose endotoxin infusion was successful in producing hyperdynamic shock. There was evidence of impaired oxidative metabolism in the liver suggesting impaired splanchnic perfusion. This may be a modifiable factor in the progression to multiple organ dysfunction and death.
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    Journal Title
    Shock
    Volume
    49
    Issue
    1
    DOI
    https://doi.org/10.1097/SHK.0000000000000904
    Copyright Statement
    © 2018 Lippincott Williams & Wilkins. This is a non-final version of an article published in final form in Shock, Volume 49 - Issue 1 - p 99–107. Reproduced in accordance with the copyright policy of the publisher. Please refer to the journal link for access to the definitive, published version.
    Subject
    Clinical sciences
    Publication URI
    http://hdl.handle.net/10072/385317
    Collection
    • Journal articles

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