Cardiac metabolism monitored by fiberoptic laser fluorimeter

1984 ◽  
Vol 108 (2) ◽  
pp. 428-429 ◽  
Author(s):  
Guy Renault ◽  
Elizabeth Raynal ◽  
Martine Sinet ◽  
Martine Muffat-Joly ◽  
Jean-Marie Vallois ◽  
...  
Keyword(s):  
Cardiac Metabolism ◽  
Laser Fluorimeter

A laser fluorimeter for direct cardiac metabolism investigation

1982 ◽  
Vol 14 (3) ◽  
pp. 143-148 ◽  
Author(s):  
G. Renault ◽  
E. Raynal ◽  
M. Sinet ◽  
J.P. Berthier ◽  
B. Godard ◽  
...  
Keyword(s):  
Cardiac Metabolism ◽  
Laser Fluorimeter

A critical perspective of the use of 13C-isotopomer analysis by GCMS and NMR as applied to cardiac metabolism

2004 ◽  
Vol 6 (1) ◽  
pp. 44-58 ◽  
Author(s):  
Christine Des Rosiers ◽  
Steven Lloyd ◽  
Blandine Comte ◽  
John C Chatham
Keyword(s):  
Cardiac Metabolism ◽  
Critical Perspective ◽  
Isotopomer Analysis ◽  
13C Isotopomer Analysis

scholarly journals Intrinsic Diurnal Variations in Cardiac Metabolism and Contractile Function

2001 ◽  
Vol 89 (12) ◽  
pp. 1199-1208 ◽  
Author(s):  
Martin E. Young ◽  
Peter Razeghi ◽  
Ari M. Cedars ◽  
Patrick H. Guthrie ◽  
Heinrich Taegtmeyer
Keyword(s):  
Contractile Function ◽  
Cardiac Metabolism ◽  
Diurnal Variations

Glucocorticoids produce whole body insulin resistance with changes in cardiac metabolism

2007 ◽  
Vol 292 (3) ◽  
pp. E654-E667 ◽  
Author(s):  
Dake Qi ◽  
Brian Rodrigues
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Glucose Utilization ◽  
Experimental Studies ◽  
Cardiac Metabolism ◽  
Multiple Organ ◽  
Whole Body ◽  
Metabolic Abnormalities ◽  
Organ Systems ◽  
Per Se

Insulin resistance is viewed as an insufficiency in insulin action, with glucocorticoids being recognized to play a key role in its pathogenesis. With insulin resistance, metabolism in multiple organ systems such as skeletal muscle, liver, and adipose tissue is altered. These metabolic alterations are widely believed to be important factors in the morbidity and mortality of cardiovascular disease. More importantly, clinical and experimental studies have established that metabolic abnormalities in the heart per se also play a crucial role in the development of heart failure. Following glucocorticoids, glucose utilization is compromised in the heart. This attenuated glucose metabolism is associated with altered fatty acid supply, composition, and utilization. In the heart, elevated fatty acid use has been implicated in a number of metabolic, morphological, and mechanical changes and, more recently, in “lipotoxicity”. In the present article, we review the action of glucocorticoids, their role in insulin resistance, and their influence in modulating peripheral and cardiac metabolism and heart disease.

Cardiac Metabolism

1965 ◽  
Vol 45 (2) ◽  
pp. 171-213 ◽  
Author(s):  
Richard J. Bing
Keyword(s):  
Cardiac Metabolism

scholarly journals Hypoxic Regulation of Hand1 Controls the Fetal-Neonatal Switch in Cardiac Metabolism

PLoS Biology ◽  
2013 ◽  
Vol 11 (9) ◽  
pp. e1001666 ◽  
Author(s):  
Ross A. Breckenridge ◽  
Izabela Piotrowska ◽  
Keat-Eng Ng ◽  
Timothy J. Ragan ◽  
James A. West ◽  
...  
Keyword(s):  
Cardiac Metabolism

Disruption of TRPV1-mediated coupling of coronary blood flow to cardiac metabolism in diabetic mice: role of nitric oxide and BK channels

2012 ◽  
Vol 303 (2) ◽  
pp. H216-H223 ◽  
Author(s):  
Giacinta Guarini ◽  
Vahagn A. Ohanyan ◽  
John G. Kmetz ◽  
Daniel J. DelloStritto ◽  
Roslin J. Thoppil ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Coronary Blood Flow ◽  
Cardiac Metabolism ◽  
Bk Channels ◽  
Bk Channel ◽  
Transient Receptor Potential Vanilloid ◽  
Trpv1 Channels ◽  
Channel Dependent

We have previously shown transient receptor potential vanilloid subtype 1 (TRPV1) channel-dependent coronary function is compromised in pigs with metabolic syndrome (MetS). However, the mechanisms through which TRPV1 channels couple coronary blood flow to metabolism are not fully understood. We employed mice lacking TRPV1 [TRPV1(−/−)], db/db diabetic, and control C57BKS/J mice to determine the extent to which TRPV1 channels modulate coronary function and contribute to vascular dysfunction in diabetic cardiomyopathy. Animals were subjected to in vivo infusion of the TRPV1 agonist capsaicin to examine the hemodynamic actions of TRPV1 activation. Capsaicin (1–100 μg·kg−1·min−1) dose dependently increased coronary blood flow in control mice, which was inhibited by the TRPV1 antagonist capsazepine or the nitric oxide synthase (NOS) inhibitor N-nitro-l-arginine methyl ester (l-NAME). In addition, the capsaicin-mediated increase in blood flow was attenuated in db/db mice. TRPV1(−/−) mice exhibited no changes in coronary blood flow in response to capsaicin. Vasoreactivity studies in isolated pressurized mouse coronary microvessels revealed a capsaicin-dependent relaxation that was inhibited by the TRPV1 inhibitor SB366791 l-NAME and to the large conductance calcium-sensitive potassium channel (BK) inhibitors iberiotoxin and Penetrim A. Similar to in vivo responses, capsaicin-mediated relaxation was impaired in db/db mice compared with controls. Changes in pH (pH 7.4–6.0) relaxed coronary vessels contracted to the thromboxane mimetic U46619 in all three groups of mice; however, pH-mediated relaxation was blunted in vessels obtained from TRPV1(−/−) and db/db mice compared with controls. Western blot analysis revealed decreased myocardial TRPV1 protein expression in db/db mice compared with controls. Our data reveal TRPV1 channels mediate coupling of myocardial blood flow to cardiac metabolism via a nitric oxide-dependent, BK channel-dependent pathway that is corrupted in diabetes.

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