Dynamic relation between myocardial contractility and energy metabolism during and following brief coronary occlusion in the pig.

Schwartz, Gregory G.; Schaefer, Saul; Meyerhoff, Dieter J.; Gober, Joel R.; Fochler, P.; Massie, Barry M.; Weiner, Michael W.

doi:10.1161/01.res.67.2.490

Cited by 27 publications

(13 citation statements)

References 45 publications

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“…This phenomenon can be attributed to the fact that ATP and CP do not represent free energy, which can be used for force generation, but only available source of this energy. It should be noted that G. Schwartz et al [122] observed a close correlation between the drop of segmentary contractility (by 24%) and the content of CP (r2=0.97), inorganic phosphate (Pi, r2=0"99) , and CP/ Pi ratio (r2=0.98) during the first few minutes of coronary occlusion. However, myocardial contractility under these conditions only little depended on ATP content: ATP utilized during systole (only 15% [105]) was rapidly resynthesized.…”

Section: Subcellular Mechanisms Of Hfmentioning

confidence: 93%

Energy, structure, conformation, and heart failure

Карсанов¹

1999

Bull Exp Biol Med

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The problem of heart failure is analyzed from the point of view of conformation changes in submolecular cardiomyocyte structures. The development of heart failure as a consequence of abnormal function of contractile myocardial proteins is discussed. The properties of actin and the role of structural changes in actin molecules in the impairment of ATP energy utilization and generation of contractile force by actomyosin complexes are studied. Experiments on animal models and autopsy samples showed that conformation changes precede disturbances in energy utilization by myofibrils, abnormal functioning of the energy-producing and Ca2+-transporting systems during the development of heart failure. It is proposed that rigid recombinations of submolecular structures in contracile proteins underlie impairment of myocardial contractility and resistance of the myocardium to regulatory factors and drugs (immobilization).Key Words: heart failure; conformation; energy; structure It is well known that severe heart failure can develop in the absence of macro-and microscopic pathognomic changes in the myocardium and vice versa patients with anatomically altered heart feel quite well, perform heavy physical work, live long, and die from noncardiac causes [29,101]. In the last case, morphological changes in the myocardium are completely compensated and the disease develops silently.Clinical symptoms, the degree of disability, and systolic and diastolic function of the myocardium [45,46,94] do not strictly correlate with structural and ultrastructural changes in cardiomyocytes [ 19,95] even in severe heart failure caused by congestive cardiomyopathy (CMP) and characterized by marked abnormalities in cardiomyocyte nucleus. T-tubular system, myofibrils, mitochondria (MC), and sarcoplasmic reticulum (SR) [67,118]. But all parameters are tended to decrease, which determine their coarse correlation [59. 94]. The absence of a strict correlation is probably due to nonspecific and nonpathognomic nature of morRepublican Research Center of Medical Biophysics. Ministry of Health of Georgia Republic, Tbilisi phological changes in CMP. These variances can be explained by the influence of compensatory mechanisms [34].Thus, the absence of a strict correlation (or at least its long latency) between functional activity of the heart and morphological changes in the myocardium as well as between functional states of the myocardium and subcellular structures responsible for the contraction-relaxation cycle [9,12,17,38,39] suggests that the main causes of FH lie beyond the resolution (beyond the sight) of not only light microscopy but also ultrastructural methods.It should be evaluated, what intracellular event(s) is(are) associated with reduced myocardial contractility.

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Section: Subcellular Mechanisms Of Hfmentioning

confidence: 93%

Energy, structure, conformation, and heart failure

Карсанов¹

1999

Bull Exp Biol Med

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“…Nonetheless, while it seems obvious that perturbation of cardiac energetics contributes to the failure of an oxygen-starved heart, the exact mechanisms underlying the decline in cardiac contractile function during oxygen deprivation remain equivocal despite decades of research (1,81). Some studies propose that depletion of high-energy phosphates [ATP and phosphocreatine (PCr)] and/or accumulation of metabolic by-products such as H ϩ , ADP, and inorganic phosphate (P i ) causes cardiac function to deteriorate (2,15,16,22,26,27,50,63,81). Others argue against such mechanisms (3,14,44,50,62).…”

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confidence: 99%

Correlation of cardiac performance with cellular energetic components in the oxygen-deprived turtle heart

Stecyk¹,

Bock²,

Overgaard³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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The relationship between cardiac energy metabolism and the depression of myocardial performance during oxygen deprivation has remained enigmatic. Here, we combine in vivo (31)P-NMR spectroscopy and MRI to provide the first temporal profile of in vivo cardiac energetics and cardiac performance of an anoxia-tolerant vertebrate, the freshwater turtle (Trachemys scripta) during long-term anoxia exposure (approximately 3 h at 21 degrees C and 11 days at 5 degrees C). During anoxia, phosphocreatine (PCr), unbound levels of inorganic phosphate (effective P(i)(2-)), intracellular pH (pH(i)), and free energy of ATP hydrolysis (dG/dxi) exhibited asymptotic patterns of change, indicating that turtle myocardial high-energy phosphate metabolism and energetic state are reset to new, reduced steady states during long-term anoxia exposure. At 21 degrees C, anoxia caused a reduction in pH(i) from 7.40 to 7.01, a 69% decrease in PCr and a doubling of effective P(i)(2-). ATP content remained unchanged, but the free energy of ATP hydrolysis (dG/dxi) decreased from -59.6 to -52.5 kJ/mol. Even so, none of these cellular changes correlated with the anoxic depression of cardiac performance, suggesting that autonomic cardiac regulation may override putative cellular feedback mechanisms. In contrast, during anoxia at 5 degrees C, when autonomic cardiac control is severely blunted, the decrease of pH(i) from 7.66 to 7.12, 1.9-fold increase of effective P(i)(2-), and 6.4 kJ/mol decrease of dG/dxi from -53.8 to -47.4 kJ/mol were significantly correlated to the anoxic depression of cardiac performance. Our results provide the first evidence for a close, long-term coordination of functional cardiac changes with cellular energy status in a vertebrate, with a potential for autonomic control to override these immediate relationships.

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“…Some studies suggest that vascular collapse may be an important mediator of contractile depression after acute no-flow ischemia (29,30). However, other studies have demonstrated a close relationship between the initial fall of pressure and energy phosphate metabolites after acute noflow ischemia, suggesting that vascular collapse is not important in mediating contractile depression (31,32).…”

Section: Discussionmentioning

confidence: 99%