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Thromboxane A2 moderates permeability after limb ischemia.

S Lelcuk, F Alexander, C R Valeri

    Annals of Surgery
    |November 1, 1985
    PubMed
    Summary
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    Thromboxane A2 (TxA2) increases microvascular permeability after limb ischemia reperfusion. Inhibiting TxA2 synthesis with OKY 046 effectively reduced this permeability, indicating its role in edema formation.

    Area of Science:

    • Vascular Biology
    • Ischemia-Reperfusion Injury
    • Pharmacology

    Background:

    • Limb ischemia reperfusion leads to muscle edema and increased vascular permeability.
    • Thromboxane A2 (TxA2) is implicated in increasing permeability in various physiological and pathological settings.

    Purpose of the Study:

    • To investigate the role of TxA2 in modulating microvascular permeability following limb ischemia.
    • To determine if inhibiting TxA2 synthesis can mitigate ischemia-induced permeability changes.

    Main Methods:

    • Hind limb ischemia was induced in dogs using a tourniquet for 2 hours.
    • Measurements included plasma and lymph levels of TxB2 (a TxA2 metabolite) and lymph/plasma protein ratio.
    • Dogs were pretreated with ketoconazole or OKY 046, imidazole derivatives that inhibit TxA2 synthesis.

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    Main Results:

    • Ischemia increased plasma and lymph TxB2 levels and lymph flow, but not the lymph/plasma protein ratio.
    • Hydrostatic pressure changes confirmed increased permeability post-ischemia.
    • OKY 046 effectively inhibited all TxA2 synthesis and maintained a lower lymph/plasma protein ratio post-ischemia compared to untreated animals.

    Conclusions:

    • Nonplatelet-derived TxA2 plays a significant role in both baseline and ischemia-induced increases in microvascular permeability.
    • Inhibition of TxA2 synthesis, particularly with OKY 046, can attenuate ischemia-induced microvascular leakiness.