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Updated: Aug 12, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
10:53

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

Published on: July 3, 2013

Influence of positive inotropic agents on intracellular calcium transients. Part II. Cardiomyopathic hamster hearts

T Stefenelli1, S T Wu, W W Parmley

  • 1Department of Medicine (Cardiology), University of California, San Francisco 94143.

American Heart Journal
|December 1, 1989
PubMed

Insights

Dobutamine worsened heart function and increased calcium in failing hearts, unlike norepinephrine and isoproterenol. This study investigates dobutamine

Area of Science:

  • Cardiology
  • Pharmacology
  • Biochemistry

Background:

  • End-stage heart failure presents complex challenges in myocardial performance.
  • Understanding the mechanisms of inotropic agents is crucial for treatment.

Purpose of the Study:

  • To investigate the effects of dobutamine on myocardial performance in end-stage heart failure.
  • To compare dobutamine's mechanism with norepinephrine and isoproterenol.

Main Methods:

  • Hemodynamic responses, high-energy phosphates (31P-NMR), and intracellular calcium ([Ca2+]i) transients were measured.
  • Syrian cardiomyopathic hamsters with severe heart failure were perfused with dobutamine, norepinephrine, or isoproterenol (10(-6) mol/L).

Main Results:

  • All agents initially increased the rate-pressure product, but dobutamine caused a subsequent decrease.
  • Dobutamine increased end-diastolic intracellular calcium ([Ca2+]i) by 19%, while norepinephrine and isoproterenol decreased it.
  • No significant differences were observed in coronary flow, pHi, high-energy phosphates, or phosphorylation potential among the agents.

Conclusions:

  • Dobutamine depressed myocardial performance in late heart failure, contrasting with norepinephrine and isoproterenol.
  • Dobutamine uniquely increased end-diastolic intracellular calcium ([Ca2+]i) in this model.

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