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Myocardial function in sepsis and endotoxin shock.

F L Abel1

  • 1Department of Physiology, University of South Carolina School of Medicine, Columbia 29208.

The American Journal of Physiology
|December 1, 1989
PubMed
Summary

Sepsis and endotoxin shock significantly impair heart muscle (myocardium) function. The exact cause of this myocardial depression remains unknown, but it involves impaired calcium transport and may deplete norepinephrine stores.

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Area of Science:

  • Cardiology
  • Pathophysiology
  • Toxicology

Background:

  • Sepsis and endotoxin shock are critical conditions affecting cardiovascular function.
  • Myocardial performance is a key determinant of outcomes in these states.
  • Previous studies have yielded varying results regarding direct myocardial damage.

Purpose of the Study:

  • To review and synthesize evidence on myocardial function during sepsis and endotoxin shock.
  • To determine if sepsis or endotoxin directly damages the myocardium.
  • To investigate the mechanisms underlying myocardial depression.

Main Methods:

  • Comparative analysis of clinical, whole animal, and isolated tissue studies.
  • Evaluation of myocardial performance considering preload, afterload, and heart rate.
  • Assessment of calcium transport, ATPase activity, and norepinephrine levels.

Main Results:

  • Overwhelming evidence indicates depressed myocardial performance in sepsis and endotoxin shock.
  • Myocardial depression is dose-related and can occur early or after a hyperdynamic phase.
  • Endotoxin itself is not the primary depressant; the active substance is unidentified.
  • Depressed calcium transport in the sarcoplasmic reticulum, particularly in the endocardium.
  • Potential depletion of myocardial ATPase and norepinephrine stores.

Conclusions:

  • Sepsis and endotoxin shock directly impair myocardial function.
  • The precise endogenous depressant substance in sepsis remains to be identified.
  • The septic myocardium exhibits increased reliance on sympathetic stimulation.
  • Inadequate coronary blood flow is unlikely to be the primary cause of myocardial depression.

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