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Left ventricular function during lethal and sublethal endotoxemia in swine.

R D Goldfarb, L M Nightingale, P Kish

    The American Journal of Physiology
    |August 1, 1986
    PubMed
    Summary
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    High doses of endotoxin significantly depressed cardiac contractility in pigs, leading to lethal outcomes. This cardiac contractile depression may be caused by reduced subendocardial blood flow.

    Area of Science:

    • Cardiovascular Physiology
    • Toxicology

    Background:

    • Endotoxin administration can cause cardiac dysfunction.
    • The canine hepatic circulation differs from humans, limiting its use in studying endotoxin effects.
    • Pigs possess a hepatic circulation similar to humans, making them a suitable model.

    Purpose of the Study:

    • To test the hypothesis that lethality after endotoxin administration is linked to cardiac contractile depression in pigs.
    • To compare cardiac mechanical function in pigs receiving high versus low doses of endotoxin.

    Main Methods:

    • Pigs were administered either a high dose (250 µg/kg) or a low dose (100 µg/kg) of endotoxin.
    • Cardiac mechanical function was assessed using the slope of the end-systolic pressure-diameter relationship (ESPDR) and other hemodynamic parameters.

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  • Plasma myocardial depressant factor activity, subendocardial blood flow, and global cardiac function were measured.

    • Main Results:

    • High-dose endotoxin caused marked, time-dependent depression of ESPDR, indicating cardiac contractile dysfunction.
    • Low-dose endotoxin did not significantly alter ESPDR.
    • Plasma myocardial depressant factor activity was elevated in endotoxin-treated pigs, particularly in the high-dose group.
    • High-dose endotoxin led to depressed subendocardial blood flow and global cardiac function, while the low dose showed non-significant increases.

    Conclusions:

    • Myocardial contractile depression is associated with lethal outcomes following high-dose endotoxin administration in pigs.
    • Reduced subendocardial blood flow is a potential mechanism contributing to endotoxin-induced cardiac dysfunction.