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An Isolated Working Heart System for Large Animal Models
Published on: June 11, 2014
The heart extrasystole: an energetic approach
F D Marengo1, M T Márquez, P Bonazzola
1Instituto de Investigaciones Cardiológicas, Facultad de Medicina y Cátedra de Biofísica, Facultad de Odontología, Universidad de Buenos Aires-Consejo Nacional de Investigaciones Científicas y Técnicas, 1122 Buenos Aires, Argentina.
The American Journal of Physiology
|January 14, 1999
Summary
An extrasystole (ES) in heart muscle primarily uses extracellular calcium, which is stored in the sarcoplasmic reticulum. This stored calcium enhances the subsequent post-extrasystolic (PES) beat, affecting cardiac energetics and calcium handling.
Area of Science:
- Cardiac Physiology
- Muscle Energetics
- Calcium Homeostasis
Background:
- Extrasystoles (ES) are premature heartbeats that can alter cardiac function.
- Understanding the energetic and calcium handling consequences of ES is crucial for cardiac health.
- Previous studies have not fully elucidated the source and fate of calcium during ES.
Purpose of the Study:
- To investigate the impact of extrasystoles (ES) on cardiac energetics and calcium (Ca2+) homeostasis in a beating heart.
- To determine the source of Ca2+ influx during ES and its subsequent handling.
- To analyze the energetic and mechanical changes in the post-extrasystolic (PES) beat.
Main Methods:
- Measurement of heat release (pressure-dependent and independent) during isovolumic contractions in arterially perfused rat ventricles.
- Analysis of heat release components (H1, H2, H3) during normal, ES, and post-extrasystolic (PES) beats.
- Investigation using caffeine pretreatment to deplete sarcoplasmic reticulum Ca2+ content.
Main Results:
- Extrasystoles (ES) introduced pressure-independent (H'2) and pressure-dependent (H'3) heat release components.
- The post-extrasystolic (PES) beat showed potentiation of pressure development and heat release, with enhanced H2 component.
- Caffeine pretreatment abolished PES potentiation, but ES mechanical and energetic outputs remained unchanged, indicating extracellular Ca2+ source for ES.
Conclusions:
- The Ca2+ influx during extrasystoles (ES) originates entirely from extracellular sources.
- Calcium entering during ES is accumulated within the sarcoplasmic reticulum.
- This SR-stored Ca2+ enhances sarcoplasmic reticulum contribution during the post-extrasystolic (PES) beat, impacting cardiac energetics.
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