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Related Experiment Videos

Monocrotaline-induced pulmonary endothelial dysfunction in rats.

A Molteni, W F Ward, C H Ts'ao

    Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)
    |May 1, 1984
    PubMed
    Summary

    Pyrrolizidine alkaloid monocrotaline causes lung injury by damaging pulmonary endothelium. This damage alters endothelial functions like angiotensin converting enzyme (ACE) activity and prostacyclin (PGI2) production, preceding structural lung abnormalities.

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    Area of Science:

    • Pulmonary Medicine
    • Toxicology
    • Endothelial Biology

    Background:

    • Pyrrolizidine alkaloids, like monocrotaline, are known toxins.
    • Endothelial damage is implicated in various lung injuries.
    • The specific role of pulmonary endothelium in monocrotaline-induced lung injury requires further elucidation.

    Purpose of the Study:

    • To investigate the role of pulmonary endothelial damage in monocrotaline-induced lung injury.
    • To assess functional changes in the pulmonary endothelium following monocrotaline exposure.
    • To correlate endothelial dysfunction with structural lung alterations.

    Main Methods:

    • Rats were administered monocrotaline (20 mg/liter) in drinking water for 1-12 weeks.
    • Pulmonary endothelial functions including angiotensin converting enzyme (ACE) activity, plasminogen activator (PLA) activity, and prostacyclin (PGI2) production were measured.

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  • Pulmonary arterial perfusion was assessed using 99mTc lung scans.
  • Lung ultrastructure was examined via electron microscopy.

    • Main Results:

    • Monocrotaline exposure led to increased ACE activity initially, followed by a decrease.
    • Plasminogen activator (PLA) activity decreased significantly after 2 weeks.
    • Prostacyclin (PGI2) production progressively increased, reaching 270% of control levels at 12 weeks.
    • Endothelial damage, edema, and inflammation were observed starting at 1-2 weeks.
    • Structural changes like increased arterial wall thickness and organ enlargement were noted at later time points.
    • Pulmonary arterial perfusion showed no significant changes.

    Conclusions:

    • Monocrotaline-induced pulmonary injury is associated with significant structural and functional abnormalities of the pulmonary endothelium.
    • Endothelial damage and dysfunction precede or accompany the development of lung injury.
    • These findings highlight the critical role of the pulmonary endothelium in the pathogenesis of monocrotaline toxicity.