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Time-dependent cardiovascular and inflammatory changes in acute endotoxemia

K Yin1, C E Hock, M Tahamont

  • 1Department of Cell Biology, University of Medicine and Dentistry, New Jersey, School of Osteopathic Medicine, Stratford 08084, USA.

Shock (Augusta, Ga.)
|June 30, 1998
PubMed
Summary

Acute endotoxemia causes cardiovascular dysfunction and lung inflammation. Superoxide generation in the lung correlates with early hemodynamic changes, while nitric oxide (NO) plays a role in later hypotension.

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Area of Science:

  • Physiology
  • Pathology
  • Pharmacology

Background:

  • Experimental acute endotoxemia involves complex cardiovascular and inflammatory responses.
  • Lipopolysaccharide (LPS) administration triggers these responses, necessitating investigation into their temporal relationship.

Purpose of the Study:

  • To examine the correlation between hemodynamic changes and pulmonary inflammatory response over time after LPS administration.
  • To measure lung and plasma nitric oxide (NO) levels and lung superoxide generation following LPS exposure.

Main Methods:

  • Administered LPS (10 mg/kg IV) to anesthetized rats and monitored hemodynamic parameters (mean arterial blood pressure, cardiac output) over time.
  • Measured plasma and lung levels of nitrite/nitrate (NO index) and lung superoxide generation at various time points post-LPS.

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  • Assessed lung histology for fluid accumulation, alveolar collapse, and leukocyte infiltration.

    • Main Results:

    • LPS induced rapid and sustained drops in mean arterial blood pressure and cardiac output.
    • Plasma NO levels significantly increased later (165 min), correlating with hypotension, while lung NO increased earlier (105 min).
    • Increased lung superoxide generation was observed early (15 min), coinciding with cardiovascular dysfunction and early lung tissue damage.

    Conclusions:

    • Early hemodynamic changes and lung tissue damage in endotoxemia may be linked to lung superoxide generation.
    • Nitric oxide (NO) appears to mediate the later hypotensive effects of LPS administration.
    • The study highlights a temporal dissociation between early superoxide-driven damage and later NO-mediated hypotension.