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Pulmonary dysfunction secondary to soft-tissue endotoxin.

H Wenger, C Wong, R H Demling

    Archives of Surgery (Chicago, Ill. : 1960)
    |February 1, 1985
    PubMed
    Summary
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    Peripheral soft tissues release thromboxane (TxB2) in response to endotoxin, causing pulmonary dysfunction like hypoxia and hypertension. Ibuprofen blocked this response, indicating TxB2

    Area of Science:

    • Physiology
    • Pharmacology
    • Pathophysiology

    Background:

    • Sepsis can lead to systemic inflammatory responses and organ dysfunction.
    • Prostanoids, such as thromboxanes and prostacyclins, are potent mediators of inflammation and vascular tone.
    • The role of peripheral soft tissues in prostanoid release during sepsis and its impact on pulmonary function remains unclear.

    Purpose of the Study:

    • To investigate if peripheral soft tissues produce and release prostanoids in response to local sepsis.
    • To determine if this mediator release contributes to pulmonary dysfunction.
    • To assess the effect of ibuprofen, a prostaglandin inhibitor, on these responses.

    Main Methods:

    • Local administration of Escherichia coli endotoxin into the flank of unanesthetized sheep.

    Related Experiment Videos

  • Measurement of thromboxane B2 (TxB2) and 6-keto-PGF1 alpha (prostacyclin) levels in tissue lymph, lung lymph, and plasma.
  • Assessment of pulmonary artery pressure (Ppa) and arterial oxygen tension (PaO2).
  • Administration of ibuprofen in a subset of animals.

    • Main Results:

    • Endotoxin induced a significant increase in TxB2 levels in tissue lymph, pulmonary artery plasma, and aortic plasma.
    • Pulmonary dysfunction, characterized by decreased PaO2 and increased Ppa, occurred after endotoxin administration.
    • Ibuprofen administration prevented the increase in TxB2 and the development of pulmonary dysfunction.

    Conclusions:

    • Peripheral soft tissues release substantial amounts of thromboxane in response to local endotoxin.
    • This thromboxane release is sufficient to cause systemic effects, including hypoxia and pulmonary hypertension.
    • The observed lung dysfunction is mediated by thromboxane and not by increased lung vascular permeability.