INVESTIGADORES
MARENGO Fernando Diego
artículos
Título:
The heart extrasystole: an energetic approach
Autor/es:
FERNANDO D. MARENGO; MARÍA T. MÁRQUEZ; PATRICIA BONAZZOLA; JORGE E. PONCE-HORNOS
Revista:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Editorial:
AMER PHYSIOLOGICAL SOC
Referencias:
Lugar: Bethesda; Año: 1999 vol. 276 p. 309 - 316
ISSN:
0363-6135
Resumen:
The consequences of an extrasystole (ES) on cardiac muscle?s energetics and Ca21 homeostasis were investigated in the beating heart. The fraction of heat release related to pressure development (pressure dependent) and pressure-independent heat release were measured during isovolumic contractions in arterially perfused rat ventricle. The heat release by a contraction showed two pressure-independent components (H1 and H2) of short evolution and a pressure-dependent component (H3). The additional heat released by ES was decomposed into one pressure-independent (H82) and one pressure-dependent (H83 )component with time courses similar to those of control components H2 and H3. ES also induced the potentiation of pressure development (P) and heat release during the postextrasystolic (PES) beat. The slope of the linear relationship between pressure-dependent heat and pressure maintenance was similar in control, ES, and PES contractions (0.08 6 0.01, 0.10 6 0.02, and 0.08 6 0.01 mJ·g21 ·mmHg21·s21, respectively). The potentiation of H2 (heat component related with Ca21 removal processes) in PES was equal to H82 at 0.3, 0.5, 1, and 2 mM Ca21, suggesting that the extra amount of Ca21 mobilized during ES was recycled in PES. Pretreatment with 1mMcaffeine to deplete sarcoplasmic reticulum Ca21 content inhibited both the mechanical and energetic potentiation of PES. However, the heat released and the pressure developed during ES were not changed by sarcoplasmic reticulum depletion. The results suggest that 1) the source of Ca21 for ES would be entirely extracellular, 2) the Ca21 entered during ES is accumulated in the sarcoplasmic reticulum, and 3) the Ca21 stored by the sarcoplasmic reticulum during ES induces an increased contribution of this organelle during PES compared with the normal contraction.