Literature DB >> 12890186

Cardiac energetics: sense and nonsense.

Colin L Gibbs1.   

Abstract

1. The background to current ideas in cardiac energetics is outlined and, in the genomic era, the need is stressed for detailed knowledge of mouse heart mechanics and energetics. 2. The mouse heart is clearly different to the rat in terms of its excitation-contraction (EC) coupling and the common assumption that heart rate difference between mice and humans will account for the eightfold difference in myocardial oxygen consumption is wrong, because the energy per beat of the mouse heart is approximately one-third that of the human heart. 3. In vivo evidence suggests that there may well be an eightfold species difference in the non-beating metabolism of mice and human hearts. It is speculated that the magnitude of basal metabolism in the heart is regulatable and that, in the absence of perfusion, it falls to approximately one-quarter of its in vivo rate and that in clinical conditions, such as hibernation, it probably decreases; its magnitude may be controlled by the endothelium. 4. The active energy balance sheet is briefly discussed and it is suggested that the activation heat accounts for 20-25% of the active energy per beat and cross-bridge turnover accounts for the balance. It is argued that force, not shortening, is the major determinant of cardiac energy usage. 5. The outcome of recent cardiac modelling with variants of the Huxley and Hill/Eisenberg models is described. It has been necessary to invoke 'loose coupling' to replicate the low cardiac energy flux measured at low afterloads (medium to high velocities of shortening). 6. Lastly, some of the unexplained or 'nonsense' energetic data are outlined and eight unsolved problems in cardiac energetics are discussed.

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Year:  2003        PMID: 12890186     DOI: 10.1046/j.1440-1681.2003.03878.x

Source DB:  PubMed          Journal:  Clin Exp Pharmacol Physiol        ISSN: 0305-1870            Impact factor:   2.557


  8 in total

1.  In vitro Models of Ischemia-Reperfusion Injury.

Authors:  Timothy Chen; Gordana Vunjak-Novakovic
Journal:  Regen Eng Transl Med       Date:  2018-05-10

2.  A new state of cardiac myosin with very slow ATP turnover: a potential cardioprotective mechanism in the heart.

Authors:  Pleuni Hooijman; Melanie A Stewart; Roger Cooke
Journal:  Biophys J       Date:  2011-04-20       Impact factor: 4.033

3.  Human Tissue-Engineered Model of Myocardial Ischemia-Reperfusion Injury.

Authors:  Timothy Chen; Gordana Vunjak-Novakovic
Journal:  Tissue Eng Part A       Date:  2018-11-20       Impact factor: 3.845

Review 4.  Contractile apparatus dysfunction early in the pathophysiology of diabetic cardiomyopathy.

Authors:  Mark T Waddingham; Amanda J Edgley; Hirotsugu Tsuchimochi; Darren J Kelly; Mikiyasu Shirai; James T Pearson
Journal:  World J Diabetes       Date:  2015-07-10

5.  Role of diastolic properties in the transition to failure in a mouse model of the cardiac dilatation.

Authors:  Peter N Costandi; Lawrence R Frank; Andrew D McCulloch; Jeffrey H Omens
Journal:  Am J Physiol Heart Circ Physiol       Date:  2006-07-21       Impact factor: 4.733

6.  Mechanosignaling pathways alter muscle structure and function by post-translational modification of existing sarcomeric proteins to optimize energy usage.

Authors:  Brenda Russell; Christopher Solís
Journal:  J Muscle Res Cell Motil       Date:  2021-02-17       Impact factor: 3.352

Review 7.  Is there a causal link between intracellular Na elevation and metabolic remodelling in cardiac hypertrophy?

Authors:  Dunja Aksentijevic; Brett A O'Brien; Thomas R Eykyn; Michael J Shattock
Journal:  Biochem Soc Trans       Date:  2018-07-03       Impact factor: 5.407

8.  Metabolites and Genes behind Cardiac Metabolic Remodeling in Mice with Type 1 Diabetes Mellitus.

Authors:  Tyler N Kambis; Hamid R Shahshahan; Paras K Mishra
Journal:  Int J Mol Sci       Date:  2022-01-26       Impact factor: 5.923

  8 in total

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