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Related Experiment Videos

Circulating negative inotropic agent(s) following pulmonary embolism.

T Utsunomiya, M K Krausz, B Dunham

    Surgery
    |April 1, 1982
    PubMed
    Summary

    Pulmonary emboli release a factor that reduces heart contractility by affecting energy availability. Indomethacin pretreatment inhibits this agent, preserving cardiac function.

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    Area of Science:

    • Cardiology
    • Pulmonary Medicine
    • Biochemistry

    Background:

    • Pulmonary emboli can mechanically impair heart function, reducing cardiac output.
    • A humoral factor released during embolism may also decrease cardiac contractility.

    Purpose of the Study:

    • To investigate the potential release of a humoral factor causing reduced cardiac contractility after pulmonary embolism.
    • To determine the effect of this factor on cardiac muscle contractility and energy metabolism.

    Main Methods:

    • Mongrel dogs were infused with clot to induce pulmonary embolism.
    • Cardiac index (CI) and stroke work (LVSW) were monitored.
    • Plasma from embolized dogs was used to assess effects on isolated rat papillary muscle and myofibril Ca++-ATPase activity.

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  • Indomethacin pretreatment was used in a subset of animals.

    • Main Results:

    • Pulmonary embolism led to decreased CI and LVSW.
    • Plasma from embolized dogs reduced papillary muscle tension and myofibril Ca++-ATPase activity.
    • A strong correlation was found between reduced contractility and decreased Ca++-ATPase activity.
    • Indomethacin pretreatment prevented the decline in LVSW and the negative effects of plasma on contractility.

    Conclusions:

    • Pulmonary emboli induce the release of a negative inotropic agent(s) affecting cardiac energy metabolism and contractility.
    • This agent's production is inhibited by indomethacin, suggesting a role for cyclooxygenase pathway products.
    • The findings highlight a humoral mechanism contributing to myocardial dysfunction post-embolism.