Metabolic reserve of the heart: The forgotten link between contraction and coronary flow

被引:32
作者
Kassiotis, Christos [1 ]
Rajabi, Mitra [1 ]
Taegtmeyer, Heinrich [1 ]
机构
[1] Univ Texas Houston, Sch Med, Dept Internal Med, Div Cardiol, Houston, TX 77030 USA
关键词
D O I
10.1016/j.pcad.2007.11.005
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Myocardial energy substrate metabolism entails a complex system of enzyme catalyzed reactions, in which the heart efficiently converts chemical to mechanical energy. The system is highly regulated and responsive to changes in workload as well as in substrate and hormone supply to the heart. Akin to the terms "contractile reserve" and "coronary flow reserve" we propose the term "metabolic reserve" to reflect the heart's capacity to respond to increases in workload. The heart's metabolic response to inotropic stimulation involves the ability to increase oxidative metabolism over a wide range, by activating the oxidation of glycogen and carbohydrate substrates. Here we review the known biochemical mechanisms responsible for those changes. Specifically, we explore the notion that disturbances in the metabolic reserve result in contractile dysfunction of the stressed heart. © 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:74 / 88
页数:15
相关论文
共 132 条
  • [1] Transcriptional coactivator PGC-1α controls the energy state and contractile function of cardiac muscle
    Arany, Z
    He, HM
    Lin, JD
    Hoyer, K
    Handschin, C
    Toka, O
    Ahmad, F
    Matsui, T
    Chin, S
    Wu, PH
    Rybkin, II
    Shelton, JM
    Manieri, M
    Cinti, S
    Schoen, FJ
    Bassel-Duby, R
    Rosenzweig, A
    Ingwall, JS
    Spiegelman, BM
    [J]. CELL METABOLISM, 2005, 1 (04) : 259 - 271
  • [2] Adaptations of skeletal muscle to exercise: rapid increase in the transcriptional coactivator PGC-1
    Baar, K
    Wende, AR
    Jones, TE
    Marison, M
    Nolte, LA
    Chen, M
    Kelly, DP
    Holloszy, JO
    [J]. FASEB JOURNAL, 2002, 16 (14) : 1879 - 1886
  • [3] Fas receptor signaling inhibits glycogen synthase kinase 3β and induces cardiac hypertrophy following pressure overload
    Badorff, C
    Ruetten, H
    Mueller, S
    Stahmer, M
    Gehring, D
    Jung, F
    Ihling, C
    Zeiher, AM
    Dimmeler, S
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 2002, 109 (03) : 373 - 381
  • [4] ACIDOSIS DURING ISCHEMIA PROMOTES ADENOSINE-TRIPHOSPHATE RESYNTHESIS IN POSTISCHEMIC RAT-HEART - IN-VIVO REGULATION OF 5'-NUCLEOTIDASE
    BAK, MI
    INGWALL, JS
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1994, 93 (01) : 40 - 49
  • [5] Deactivation of peroxisome proliferator-activated receptor-α during cardiac hypertrophic growth
    Barger, PM
    Brandt, JM
    Leone, TC
    Weinheimer, CJ
    Kelly, DP
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 2000, 105 (12) : 1723 - 1730
  • [6] PPAR signaling in the control of cardiac energy metabolism
    Barger, PM
    Kelly, DP
    [J]. TRENDS IN CARDIOVASCULAR MEDICINE, 2000, 10 (06) : 238 - 245
  • [7] Bartelds B, 2000, CIRCULATION, V102, P926, DOI 10.1161/01.CIR.102.8.926
  • [8] Relative importance of malonyl CoA and carnitine in maturation of fatty acid oxidation in newborn rabbit heart
    Besikci, AO
    Campbell, FM
    Hopkins, TA
    Dyck, JRB
    Lopaschuk, GD
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2003, 284 (01): : H283 - H289
  • [9] STUDIES ON MYOCARDIAL METABOLISM .6. MYOCARDIAL METABOLISM IN CONGESTIVE FAILURE
    BLAIN, JM
    SCHAFER, H
    SIEGEL, AL
    BING, RJ
    [J]. AMERICAN JOURNAL OF MEDICINE, 1956, 20 (06) : 820 - 833
  • [10] Bonow RO, 1999, J AM COLL CARDIOL, V33, P705