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Related Experiment Videos

Cardiac myofilament protein function is altered during sepsis

F M Powers1, S Farias, H Minami

  • 1Research Services, West Side VA Hospital, Chicago, IL, USA.

Journal of Molecular and Cellular Cardiology
|June 10, 1998
PubMed
Summary

Sepsis alters heart muscle function by changing myofilament ATPase activity, not protein levels. These biochemical changes in cardiac muscle may explain ventricular dysfunction during prolonged sepsis.

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Area of Science:

  • Cardiology
  • Biochemistry
  • Physiology

Background:

  • Sepsis can lead to cardiac dysfunction.
  • The underlying molecular mechanisms affecting cardiac myofilaments during sepsis are not fully understood.

Purpose of the Study:

  • To investigate alterations in cardiac myofilament protein levels and function during chronic peritoneal sepsis in a rat model.
  • To determine if changes in myofilament ATPase activity or Ca(2+) sensitivity contribute to sepsis-induced ventricular dysfunction.

Main Methods:

  • Male Sprague-Dawley rats underwent cecal material injection to induce sepsis.
  • Ventricular function was assessed in isolated hearts on days 1, 3, and 7 post-sepsis.
  • Myofilament protein levels were analyzed using SDS-PAGE.
  • Myofilament ATPase activities (Ca(2+)-independent Mg-ATPase, maximal ATPase, K(EDTA)-, Ca(2+)-, and Mg(2+)-ATPase) were measured.

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Main Results:

  • Ventricular function was depressed on days 3 and 7 of sepsis.
  • No significant changes in the relative amounts of key myofilament proteins (actin, troponin, tropomyosin, myosin light chains) were observed.
  • Ca(2+)-independent Mg-ATPase activity was elevated on days 1 and 3, while maximal ATPase activity increased on days 3 and 7.
  • Myofilament Ca(2+) sensitivity was altered during sepsis.

Conclusions:

  • Chronic peritoneal sepsis induces alterations in cardiac myofilament ATPase activities and Ca(2+) sensitivity.
  • These biochemical changes in myofilaments, rather than altered protein levels, likely contribute to the observed depression in ventricular function during sepsis.