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Related Experiment Videos

Polymorphonuclear leukocyte: arachidonate edema.

D M Shasby, S S Shasby, M J Peach

    Journal of Applied Physiology (Bethesda, Md. : 1985)
    |July 1, 1985
    PubMed
    Summary
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    Polymorphonuclear leukocytes (PMN) and arachidonate interact to increase lung vascular permeability. PMN cyclooxygenase activity is crucial for this edematous process, impacting acute lung inflammation.

    Area of Science:

    • Pulmonary Medicine
    • Cell Biology
    • Inflammation Research

    Background:

    • Polymorphonuclear leukocytes (PMN) and enhanced arachidonate metabolism are implicated in acute lung edema.
    • Alveolar capillary permeability and endothelial barrier function are critical in lung fluid balance.

    Purpose of the Study:

    • To investigate the interaction between PMN and arachidonate in increasing alveolar capillary permeability.
    • To determine the role of PMN cyclooxygenase activity in the edematous process.

    Main Methods:

    • Isolated perfused lungs and cultured endothelial cell monolayers were used to assess alveolar capillary permeability.
    • Experiments involved the addition of PMN and arachidonate, with and without inhibitors of PMN or endothelial cyclooxygenase, proteases, and oxidants.

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  • Leukotriene synthesis inhibition and direct leukotriene addition were also tested.

    • Main Results:

    • PMN and arachidonate together, but not alone, increased lung vascular permeability and albumin transfer across endothelial cells.
    • Inhibition of PMN cyclooxygenase, but not endothelial cyclooxygenase, significantly reduced the edematous effect.
    • PMN proteases, PMN-derived oxidants, and leukotrienes were not found to be directly involved in this specific edematogenic activity.

    Conclusions:

    • PMN and arachidonate interact to enhance endothelial permeability in the lung vasculature.
    • PMN cyclooxygenase activity plays a critical role in mediating this PMN-arachidonate-induced increase in permeability.
    • This interaction is a significant factor in acute inflammatory processes within the lung vasculature.