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Published on: April 21, 2014
Cardiac hypertrophy determines digitalis action on intracellular Ca2+ in human myocardium
J R Lopez1, N Linares, P A Brady
1Centro de Biofisica y Bioquimica, Instituto Venezolano de Investigaciones Cientificas, Caracas, Venezuela.
Insights
Ventricular hypertrophy increases intracellular calcium levels more significantly when treated with digitalis (strophanthidin). The degree of hypertrophy inversely impacts this calcium increase in human heart muscle.
Area of Science:
- Cardiology
- Biochemistry
- Physiology
Background:
- Ventricular hypertrophy alters ion transporters crucial for digitalis efficacy.
- The effect of digitalis on intracellular cations in hypertrophied human myocardium is not well understood.
Purpose of the Study:
- To investigate the impact of digitalis (strophanthidin) on intracellular calcium (Ca2+) levels in human myocardium with and without ventricular hypertrophy.
- To determine how ventricular hypertrophy influences the response to digitalis treatment.
Main Methods:
- Utilized double-barreled Ca2+-selective microelectrodes to measure Ca2+ activity and membrane potential.
- Analyzed myocardial samples from patients with and without ventricular hypertrophy before and after strophanthidin exposure.
Main Results:
- Ventricular hypertrophy led to a greater increase in diastolic Ca2+ levels upon strophanthidin exposure compared to non-hypertrophied samples.
- The increase in Ca2+ induced by strophanthidin was inversely proportional to the myocardial mass in hypertrophied hearts.
Conclusions:
- The extent of ventricular hypertrophy dictates the digitalis-induced changes in intracellular Ca2+ within the human myocardium.
- Findings highlight the importance of considering myocardial hypertrophy when assessing digitalis treatment outcomes.
Abstract:
Ventricular hypertrophy alters transporters associated with digitalis action, but the outcome of digitalis treatment on intracellular cations in the hypertrophied human myocardium remains unknown. Using double-barreled Ca2+-selective microelectrodes, we simultaneously measured Ca2+ activity and membrane potential in myocardial samples from patients without and with ventricular hypertrophy, prior to and following exposure to strophanthidin, a prototype digitalis. We found that ventricular hypertrophy is associated with greater strophanthidin-induced increase in diastolic Ca2+ levels compared to that observed in the absence of hypertrophy. Furthermore, in hypertrophied myocardium the magnitude of the increase in Ca2+ induced by strophanthidin was inversely related to increase in myocardial mass. Thus, the extent of ventricular hypertrophy determines digitalis action on intracellular Ca2+ within the human myocardium.
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