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Monocrotaline pneumotoxicity in mice.

A Molteni1, W F Ward, C H Ts'ao

  • 1Department of Pathology, Northwestern University School of Medicine, Chicago, IL 60611.

Virchows Archiv. B, Cell Pathology Including Molecular Pathology
|January 1, 1989
PubMed
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Mice exposed to monocrotaline, a pyrrolizidine alkaloid, showed dose-dependent lung endothelial dysfunction and inflammation. However, unlike rats, mice exhibited minimal pulmonary hypertension and fibrosis, indicating species-specific responses to monocrotaline toxicity.

Area of Science:

  • Toxicology
  • Pulmonary Medicine
  • Cardiovascular Research

Background:

  • The pyrrolizidine alkaloid monocrotaline (MCT) is a known inducer of lung injury and pulmonary hypertension in rats.
  • The effects and quantitation of MCT-induced cardiopulmonary injury in mice have been less extensively studied.

Purpose of the Study:

  • To investigate and quantitate the effects of MCT on pulmonary endothelial function, inflammation, and cardiac remodeling in mice.
  • To compare the toxicological responses of mice to MCT with those previously observed in rats.

Main Methods:

  • Adult male mice received varying doses of MCT (2.4, 4.8, or 24.0 mg/kg/day) in drinking water for 6 weeks.
  • Pulmonary endothelial function was assessed via lung angiotensin converting enzyme (ACE) and plasminogen activator (PLA) activities, and prostacyclin (PGI2) and thromboxane (TXA2) production.

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  • Lung histology (light and electron microscopy) and cardiac right ventricular hypertrophy (RV/LV + S ratio) were evaluated.

    • Main Results:

    • MCT induced a dose-dependent decrease in lung ACE and PLA activities and an increase in PGI2 and TXA2 production, indicating endothelial dysfunction, significant only at the highest dose.
    • Histological examination revealed dose-dependent pulmonary inflammatory and exudative reactions.
    • Mice showed minimal lung fibrosis, cardiomegaly, or right ventricular hypertrophy, and no occlusive medial thickening of pulmonary arteries, even at high doses.

    Conclusions:

    • Mice exhibit significant quantitative biochemical and qualitative morphological differences in response to MCT pneumotoxicity compared to rats.
    • In mice, MCT-induced lung endothelial dysfunction and inflammation appear dissociated from the development of pulmonary hypertension and fibrosis.
    • These findings highlight species-specific differences in susceptibility and response to MCT, impacting its utility as a model for pulmonary hypertension research.