BIOMAT Database Logo BIOMAT Database Logo

Myocardial creatine kinase kinetics in hearts with postinfarction left ventricular remodeling. 1999

Y Murakami, and J Zhang, and M H Eijgelshoven, and W Chen, and W C Carlyle, and Y Zhang, and G Gong, and R J Bache
Department of Medicine and Center for Magnetic Resonance Research, University of Minnesota, Minneapolis, Minnesota 55455, USA.

This study examined whether alterations in myocardial creatine kinase (CK) kinetics and high-energy phosphate (HEP) levels occur in postinfarction left ventricular remodeling (LVR). Myocardial HEP and CK kinetics were examined in 19 pigs 6 wk after myocardial infarction was produced by left circumflex coronary artery ligation, and the results were compared with those from 9 normal pigs. Blood flow (microspheres), oxygen consumption (MVO2), HEP levels [31P magnetic resonance spectroscopy (MRS)], and CK kinetics (31P MRS) were measured in myocardium remote from the infarct under basal conditions and during dobutamine infusion (20 micrograms. kg-1. min-1 iv). Six of the pigs with LVR had overt congestive heart failure (CHF) at the time of study. Under basal conditions, creatine phosphate (CrP)-to-ATP ratios were lower in all transmural layers of hearts with CHF and in the subendocardium of LVR hearts than in normal hearts (P < 0.05). Myocardial ATP (biopsy) was significantly decreased in hearts with CHF. The CK forward rate constant was lower (P < 0.05) in the CHF group (0.21 +/- 0.03 s-1) than in LVR (0.38 +/- 0.04 s-1) or normal groups (0.41 +/- 0.03 s-1); CK forward flux rates in CHF, LVR, and normal groups were 6.4 +/- 2.3, 14.3 +/- 2.1, and 20.3 +/- 2.4 micromol. g-1. s-1, respectively (P < 0.05, CHF vs. LVR and LVR vs. normal). Dobutamine caused doubling of the rate-pressure product in the LVR and normal groups, whereas CHF hearts failed to respond to dobutamine. CK flux rates did not change during dobutamine in any group. The ratios of CK flux to ATP synthesis (from MVO2) under baseline conditions were 10.9 +/- 1.2, 8. 03 +/- 0.9, and 3.86 +/- 0.5 for normal, LVR, and CHF hearts, respectively (each P < 0.05); during dobutamine, this ratio decreased to 3.73 +/- 0.5, 2.58 +/- 0.4, and 2.78 +/- 0.5, respectively (P = not significant among groups). These data demonstrate that CK flux rates are decreased in hearts with postinfarction LVR, but this change does not limit the response to dobutamine. In hearts with end-stage CHF, the changes in HEP and CK flux are more marked. These changes could contribute to the decreased responsiveness of these hearts to dobutamine.

UI MeSH Term Description Entries
D007700 Kinetics The rate dynamics in chemical or physical systems.
D009203 Myocardial Infarction NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION). Cardiovascular Stroke,Heart Attack,Myocardial Infarct,Cardiovascular Strokes,Heart Attacks,Infarct, Myocardial,Infarction, Myocardial,Infarctions, Myocardial,Infarcts, Myocardial,Myocardial Infarctions,Myocardial Infarcts,Stroke, Cardiovascular,Strokes, Cardiovascular
D009206 Myocardium The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow. Muscle, Cardiac,Muscle, Heart,Cardiac Muscle,Myocardia,Cardiac Muscles,Heart Muscle,Heart Muscles,Muscles, Cardiac,Muscles, Heart
D009682 Magnetic Resonance Spectroscopy Spectroscopic method of measuring the magnetic moment of elementary particles such as atomic nuclei, protons or electrons. It is employed in clinical applications such as NMR Tomography (MAGNETIC RESONANCE IMAGING). In Vivo NMR Spectroscopy,MR Spectroscopy,Magnetic Resonance,NMR Spectroscopy,NMR Spectroscopy, In Vivo,Nuclear Magnetic Resonance,Spectroscopy, Magnetic Resonance,Spectroscopy, NMR,Spectroscopy, Nuclear Magnetic Resonance,Magnetic Resonance Spectroscopies,Magnetic Resonance, Nuclear,NMR Spectroscopies,Resonance Spectroscopy, Magnetic,Resonance, Magnetic,Resonance, Nuclear Magnetic,Spectroscopies, NMR,Spectroscopy, MR
D010101 Oxygen Consumption The rate at which oxygen is used by a tissue; microliters of oxygen STPD used per milligram of tissue per hour; the rate at which oxygen enters the blood from alveolar gas, equal in the steady state to the consumption of oxygen by tissue metabolism throughout the body. (Stedman, 25th ed, p346) Consumption, Oxygen,Consumptions, Oxygen,Oxygen Consumptions
D010758 Phosphorus A non-metal element that has the atomic symbol P, atomic number 15, and atomic weight 31. It is an essential element that takes part in a broad variety of biochemical reactions. Black Phosphorus,Phosphorus-31,Red Phosphorus,White Phosphorus,Yellow Phosphorus,Phosphorus 31,Phosphorus, Black,Phosphorus, Red,Phosphorus, White,Phosphorus, Yellow
D003326 Coronary Circulation The circulation of blood through the CORONARY VESSELS of the HEART. Circulation, Coronary
D003402 Creatine Kinase A transferase that catalyzes formation of PHOSPHOCREATINE from ATP + CREATINE. The reaction stores ATP energy as phosphocreatine. Three cytoplasmic ISOENZYMES have been identified in human tissues: the MM type from SKELETAL MUSCLE, the MB type from myocardial tissue and the BB type from nervous tissue as well as a mitochondrial isoenzyme. Macro-creatine kinase refers to creatine kinase complexed with other serum proteins. Creatine Phosphokinase,ADP Phosphocreatine Phosphotransferase,ATP Creatine Phosphotransferase,Macro-Creatine Kinase,Creatine Phosphotransferase, ATP,Kinase, Creatine,Macro Creatine Kinase,Phosphocreatine Phosphotransferase, ADP,Phosphokinase, Creatine,Phosphotransferase, ADP Phosphocreatine,Phosphotransferase, ATP Creatine
D006439 Hemodynamics The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM. Hemodynamic
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia

Related Publications

Y Murakami, and J Zhang, and M H Eijgelshoven, and W Chen, and W C Carlyle, and Y Zhang, and G Gong, and R J Bache
31P NMR 2D Mapping of Creatine Kinase Forward Flux Rate in Hearts with Postinfarction Left Ventricular Remodeling in Response to Cell Therapy.
January 2016, PloS one,
Y Murakami, and J Zhang, and M H Eijgelshoven, and W Chen, and W C Carlyle, and Y Zhang, and G Gong, and R J Bache
[Postinfarction left ventricular remodeling in patients with hypertension].
January 2004, Kardiologiia,
Y Murakami, and J Zhang, and M H Eijgelshoven, and W Chen, and W C Carlyle, and Y Zhang, and G Gong, and R J Bache
Nicotine-modified postinfarction left ventricular remodeling.
March 1999, The American journal of physiology,
Y Murakami, and J Zhang, and M H Eijgelshoven, and W Chen, and W C Carlyle, and Y Zhang, and G Gong, and R J Bache
[Postinfarction remodeling and left ventricular aneurysm].
January 2007, Klinicheskaia meditsina,
Y Murakami, and J Zhang, and M H Eijgelshoven, and W Chen, and W C Carlyle, and Y Zhang, and G Gong, and R J Bache
Gender differences in postinfarction left ventricular remodeling.
January 1999, Cardiology,
Y Murakami, and J Zhang, and M H Eijgelshoven, and W Chen, and W C Carlyle, and Y Zhang, and G Gong, and R J Bache
Chronic high-dose creatine feeding does not attenuate left ventricular remodeling in rat hearts post-myocardial infarction.
July 1999, Cardiovascular research,
Y Murakami, and J Zhang, and M H Eijgelshoven, and W Chen, and W C Carlyle, and Y Zhang, and G Gong, and R J Bache
Rat Left Ventricular Cardiomyocytes Characterization in the Process of Postinfarction Myocardial Remodeling.
July 2019, Cytometry. Part A : the journal of the International Society for Analytical Cytology,
Y Murakami, and J Zhang, and M H Eijgelshoven, and W Chen, and W C Carlyle, and Y Zhang, and G Gong, and R J Bache
Creatine kinase knockout mice show left ventricular hypertrophy and dilatation, but unaltered remodeling post-myocardial infarction.
February 2005, Cardiovascular research,
Y Murakami, and J Zhang, and M H Eijgelshoven, and W Chen, and W C Carlyle, and Y Zhang, and G Gong, and R J Bache
Myocardial creatine kinase expression after left ventricular assist device support.
June 2002, Journal of the American College of Cardiology,
Y Murakami, and J Zhang, and M H Eijgelshoven, and W Chen, and W C Carlyle, and Y Zhang, and G Gong, and R J Bache
Bioenergetic and functional consequences of bone marrow-derived multipotent progenitor cell transplantation in hearts with postinfarction left ventricular remodeling.
April 2007, Circulation,
Copied contents to your clipboard!