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Decrease in left ventricular contractility after tumor necrosis factor-alpha infusion in dogs

K R Walley1, P C Hebert, Y Wakai

  • 1Pulmonary Research Laboratory, St. Paul's Hospital, Vancouver, British Columbia, Canada.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|March 1, 1994
PubMed
Summary
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Tumor necrosis factor-alpha (TNF-alpha) rapidly depresses left ventricular contractility, leading to a hypotensive, hyperdynamic circulation. This study reveals TNF-alpha as a key factor in sepsis-induced myocardial depression.

Area of Science:

  • Cardiovascular Physiology
  • Immunology
  • Sepsis Pathophysiology

Background:

  • Sepsis is characterized by circulatory dysfunction, but the early cardiac effects of key mediators like tumor necrosis factor-alpha (TNF-alpha) remain unclear.
  • Understanding the temporal relationship between TNF-alpha exposure and changes in cardiac function is crucial for sepsis management.

Purpose of the Study:

  • To investigate whether systolic contractility or diastolic compliance is altered early after TNF-alpha administration.
  • To determine the role of TNF-alpha in the hypotensive and hyperdynamic circulatory state observed in sepsis.

Main Methods:

  • Hemodynamic parameters, left ventricular contractility (end-systolic pressure-volume relationship), and diastolic pressure-volume relationships were measured in dogs.
  • Dogs received intravenous infusion of TNF-alpha (60 µg.kg⁻¹.h⁻¹) or served as controls.

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Main Results:

  • TNF-alpha infusion caused a significant decrease in mean aortic pressure and a significant increase in cardiac output within 1 hour.
  • Left ventricular contractility decreased by 23% at 1 hour and 52% at 5 hours post-TNF-alpha infusion.
  • Diastolic pressure-volume relationships remained unchanged, and ejection fraction was preserved due to decreased afterload.

Conclusions:

  • TNF-alpha significantly contributes to the hypotensive and hyperdynamic circulation characteristic of sepsis.
  • Early depression of left ventricular contractility following TNF-alpha exposure identifies it as a potential myocardial depressant factor in sepsis.