Jorge E. Ponce-Hornos

Tension-dependent and tension-independent energy components of heart contraction

Heat production and isovolumetric pressure development (P) were measured simultaneously in the arterially perfused rat ventricle. The time course of the calorimetric signal that follows a contraction could be decomposed into four components of energy released. Three of these components (H1, H2, and H4) were pressure independent, only H3 correlated with either P or the pressure-time integral (PtI) (r>0.78, n=36, P<0.01). The dimensionless slope of the regression of H3 on P was 0.24 (an index of muscle economy) and the absence of O2 (N2 replacement) decreased it to 0.178 suggesting that 26% of H3 is related to oxidative metabolism. H4 was the most affected by the lack of O2 in the perfusate. It decreased to 16% in the first beat under N2 without change in P or in H1, H2 or H3, and disappeared (1.6±1.0 mJ.g−1) in the fourth contraction under N2 (while P, H1, H2 and H3 remained over 64% of their control values). H4 was activated during the first 1–3 beats after a quiescent period and remained active for several seconds (even in the absence of subsequent stimulation) as if the basal metabolism had been increased to a new steady level. H1 and H2 were dependent on the extracellular Ca. The magnitudes of both H1 (1.8±0.2 mJ.g−1) and H2 (2.7±0.2 mJ.g−1) were similar to those reported for the fast and slow components of activation heat in skeletal muscle. If twin stimuli are applied (200 ms apart), additional energy is released (+3.0±0.3 mJ.g−1) that can be decomposed in two components similar to those identified as H2 and H3. The magnitude of H1, its absence in the twin contraction and its Ca dependency suggest an association with Ca-binding processes (mainly Troponin C). The presence of an H2 component during the twin contraction, its magnitude and Ca dependence gives support to a relationship between H2 and Ca removal processes.

The heart extrasystole: an energetic approach

The consequences of an extrasystole (ES) on cardiac muscles energetics and Ca2+ 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 ([Formula: see text]) and one pressure-dependent ([Formula: see text]) 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 ± 0.01, 0.10 ± 0.02, and 0.08 ± 0.01 mJ ⋅ g-1 ⋅ mmHg-1 ⋅ s-1, respectively). The potentiation of H2 (heat component related with Ca2+ removal processes) in PES was equal to [Formula: see text] at 0.3, 0.5, 1, and 2 mM Ca2+, suggesting that the extra amount of Ca2+ mobilized during ES was recycled in PES. Pretreatment with 1 mM caffeine to deplete sarcoplasmic reticulum Ca2+ 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 Ca2+ for ES would be entirely extracellular, 2) the Ca2+ entered during ES is accumulated in the sarcoplasmic reticulum, and 3) the Ca2+ stored by the sarcoplasmic reticulum during ES induces an increased contribution of this organelle during PES compared with the normal contraction.

Energetics of heart muscle contraction under high K perfusion: verapamil and Ca effects

Tension-dependent (TDH) and tension-independent heat (TIH) release were measured during single isovolumetric contractions in the arterially perfused rat ventricle. Under perfusion with 7 mM K-0.5 mM Ca, TDH showed only one component (H3), whereas TIH could be divided into two components (H1 and H2) of short evolution (similar to the classically identified activation heat) and one component (H4) of long duration (dependent on mitochondrial respiration). Under 25 mM K, TIH components (i.e., H1, H2, and H4) increased with the increase in extracellular Ca concentration ([Ca]o) from 0.5 to 4 mM, and H3 correlated with pressure at all [Ca]o, with regression parameters similar to those observed under 7 mM K. Under 25 mM K-2 mM Ca, peak pressure development (P), H1, H2, and H3, plotted against the number of beats under 0.4 μM verapamil, exponentially decreased, but H4 decreased to 5.5 ± 2.9% in the first contraction and remained constant thereafter. Under hypoxia, P, H1, H2, and H3 progressively decreased for about six contractions, but H4 was not detectable from the second contraction. The results suggest that increasing extracellular K concentration decreases contractile economy mainly by increasing energy expenditure related to a Ca-dependent (verapamil-sensitive) mitochondrial activity that is not related to force generation.Tension-dependent (TDH) and tension-independent heat (TIH) release were measured during single isovolumetric contractions in the arterially perfused rat ventricle. Under perfusion with 7 mM K-0.5 mM Ca, TDH showed only one component (H3), whereas TIH could be divided into two components (H1 and H2) of short evolution (similar to the classically identified activation heat) and one component (H4) of long duration (dependent on mitochondrial respiration). Under 25 mM K, TIH components (i.e., H1, H2, and H4) increased with the increase in extracellular Ca concentration ([Ca]o) from 0.5 to 4 mM, and H3 correlated with pressure at all [Ca]o, with regression parameters similar to those observed under 7 mM K. Under 25 mM K-2 mM Ca, peak pressure development (P), H1, H2, and H3, plotted against the number of beats under 0.4 microM verapamil, exponentially decreased, but H4 decreased to 5.5 +/- 2.9% in the first contraction and remained constant thereafter. Under hypoxia, P, H1, H2, and H3 progressively decreased for about six contractions, but H4 was not detectable from the second contraction. The results suggest that increasing extracellular K concentration decreases contractile economy mainly by increasing energy expenditure related to a Ca-dependent (verapamil-sensitive) mitochondrial activity that is not related to force generation.

The role of extracellular sodium on heart muscle energetics

AbstractA study has been made of changing external sodium concentration [Na]e, over the range 75 to 200 mmol · l−1, on contractile parameters and heat production in isolated, arterially perfused, interventricular rabbit septa.-The observed changes in maximum rate of contraction with [Na]e, either in the presence of a constant external Ca concentration [Ca]e or in the presence of a constant [Na]e2/[Ca]e ratio, paralleled those observed for tension development (T). On the other hand the maximal rate of relaxation

Influence of extracellular potassium on energetics of resting heart muscle

\left( { - \dot T_{\max } } \right)

Lithium and KB-R7943 effects on mechanics and energetics of rat heart muscle.

and the ratio

Role of extracellular calcium on heart muscle energetics: effects of verapamil

- \dot T_{\max } /T