Cardiac Efficiency: Who's Got the Power?

2020 ◽  
Vol 21 (11) ◽  
pp. 1334-1335
Author(s):  
Steven J. Yakubov ◽  
Anupam Basuray ◽  
Carlos S. Sanchez
Keyword(s):  
Cardiac Efficiency

Matching the Heart to Heat-Induced Circulatory Load: Heat-Acclimatory Responses

Physiology ◽  
2003 ◽  
Vol 18 (6) ◽  
pp. 215-221 ◽  
Author(s):  
Michal Horowitz
Keyword(s):  
Heart Rate ◽  
Oxygen Demand ◽  
Heat Acclimation ◽  
Regulatory Proteins ◽  
Contractile Apparatus ◽  
Cardiac Efficiency ◽  
Cross Tolerance ◽  
Altered Expression ◽  
Expression Of Genes ◽  
Cardiac Adaptation

Heat acclimation enhances cardiac efficiency by increasing stroke volume and decreasing heart rate. These adaptations involve biochemical changes in the contractile apparatus, switched on by altered expression of genes coding contractile and calcium-regulatory proteins and partially mediated by persistent low thyroxine. Heat acclimation also produces cross-tolerance to oxygen deprivation, thus reinforcing cardiac adaptation to oxygen demand/supply mismatching via energy-sparing pathways.

Abstract 282: Adropin Enhancement of Cardiac Insulin Sensitivity and Inhibition of Fatty Acid Oxidation are Associated With Improvement of Cardiac Function and Efficiency in Hearts From Fasted Mice

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Tariq R Altamimi ◽  
Arata Fukushima ◽  
Liyan Zhang ◽  
Su Gao ◽  
Abhishek Gupta ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Diabetic Cardiomyopathy ◽  
Insulin Signaling ◽  
Plasma Levels ◽  
Acid Oxidation ◽  
Post Translational Modification ◽  
Cardiac Efficiency ◽  
Oxidation Rates ◽  
Cardiac Energy

Impaired cardiac insulin signaling and high cardiac fatty acid oxidation rates are characteristics of diabetic cardiomyopathy. Potential roles for liver-derived metabolic factors in mediating cardiac energy homeostasis are underappreciated. Plasma levels of adropin, a liver secreted peptide, increase during feeding and decrease during fasting and diabetes. In skeletal muscle, adropin preferentially promotes glucose over fatty acid oxidation. We therefore determined what effect adropin has on cardiac energy metabolism, insulin signaling and cardiac efficiency. C57Bl/6 mice were fasted to accentuate the differences in adropin plasma levels between animals injected 3 times over 24 hr with either vehicle or adropin (450 nmol/kg i.p.). Despite fasting-induced predominance of fatty acid oxidation measured in isolated working hearts, insulin inhibition of fatty acid oxidation was re-established in adropin-treated mice (from 1022±143 to 517±56 nmol. g dry wt -1 . min -1 , p <0.05) compared to vehicle-treated mice (from 757±104 to 818±103 nmol. g dry wt -1 . min -1 ). Adropin-treated mice hearts showed higher cardiac work over the course of perfusion (p<0.05 vs. vehicle), which was accompanied by improved cardiac efficiency and enhanced phosphorylation of insulin signaling enzymes (tyrosine-IRS-1, AS160, p<0.05). Acute addition of adropin (2nM) to isolated working hearts from non-fasting mice showed a robust stimulation of glucose oxidation compared to vehicle-treated hearts (3025±401 vs 1708±292 nmol. g dry wt -1 . min -1 , p<0.05, respectively) with a corresponding inhibition of palmitate oxidation (325±61 vs 731±160 nmol. g dry wt -1 . min -1 , p<0.05, respectively), even in the presence of insulin. Acute adropin addition to hearts also increased IRS-1 tyrosine-phosphorylation as well as Akt, and GSK3β phosphorylation (p<0.05), suggesting acute receptor- and/or post-translational modification-mediated mechanisms. These results suggest adropin as a putative candidate for the treatment of diabetic cardiomyopathy.

Abstract 15649: Pharmacological Inhibition of Aldose Reductase by AT001 Prevents Abnormal Cardiac Energy Metabolism and Improves Heart Function in an Animal Model of Diabetic Cardiomyopathy

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Keshav Gopal ◽  
Qutuba Karwi ◽  
Seyed Amirhossein Tabatabaei Dakhili ◽  
Riccardo Perfetti ◽  
Ravichandran Ramasamy ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Energy Metabolism ◽  
Fatty Acid Oxidation ◽  
Diabetic Cardiomyopathy ◽  
Acid Oxidation ◽  
Cardiac Energetics ◽  
Cardiac Efficiency ◽  
Oxidation Rates ◽  
Cardiac Energy Metabolism ◽  
Cardiac Energy

Introduction: Diabetic Cardiomyopathy (DCM) is a major cause of death in people with type 2 diabetes (T2D). Alterations in cardiac energy metabolism including increased fatty acid oxidation rates and reduced glucose oxidation rates are key contributing factors to the development of DCM. Studies have shown that Aldose Reductase (AR), an enzyme activated under hyperglycemic conditions, can modulate myocardial glucose and fatty acid oxidation, and promotes cardiac dysfunction. Hypothesis: Pharmacological inhibition of AR using a next-generation inhibitor AT-001, can mitigate DCM in mice by modulating cardiac energy metabolism and improving cardiac efficiency. Methods: Male human AR overexpressing (hAR-Tg) and C57BL/6J (Control) mice were subjected to experimental T2D (high-fat diet [60% kcal from lard] for 10-wk with a single intraperitoneal streptozotocin injection of 75 mg/kg) and treated for the last 3-wk with AT-001 (40mg/kg/day) or vehicle via oral gavage. Cardiac energy metabolism and in vivo cardiac function were assessed via isolated working heart perfusions and ultrasound echocardiography, respectively. Results: AT-001 treatment significantly improved cardiac energetics in a murine model of DCM (hAR-Tg mice with T2D). Particularly, AT-001-treated mice exhibited decreased cardiac fatty acid oxidation rates compared to the vehicle-treated mice (342 ± 53 vs 964 ± 130 nmol/min/g dry wt.). Concurrently, there was a significant decrease in cardiac oxygen consumption in the AT-001-treated compared to the vehicle-treated mice (41 ± 12 vs 60 ± 11 μmol/min/g dry wt.), suggesting increased cardiac efficiency. Furthermore, treatment with AT-001 prevented cardiac structural and functional abnormalities present in DCM, including diastolic dysfunction as reflected by an increase in the tissue Doppler E’/A’ ratio and decrease in E/E’ ratio. Moreover, AT-001 treatment prevented cardiac hypertrophy as reflected by a decrease in LV mass in AT-001-treated mice. Conclusions: AR inhibition with AT-001 prevents cardiac structural and functional abnormalities in a mouse model of DCM, and normalizes cardiac energetics by shifting cardiac metabolism towards a non-diabetic metabolic state.

Abstract 062: Mitoubiquinone Decreases Reactive Oxygen Species Production and Improves Cardiac Efficiency in Chronic Volume Overload

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Danielle M Yancey ◽  
James D Gladden ◽  
Jason L Guichard ◽  
Victor M Darley-Usmar ◽  
Louis J Dell’Italia ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Membrane Potential ◽  
Systolic Pressure ◽  
Reactive Oxygen ◽  
Volume Overload ◽  
Left Ventricular ◽  
Ros Production ◽  
Oxygen Species ◽  
Cardiac Efficiency ◽  
Lv Dysfunction

Background: The hemodynamic stress of left ventricular (LV) volume overload (VO) produces LV dysfunction accompanied by mitochondrial and cytoskeletal disruption in cardiomyocytes. Because mitochondria are both a source and target of reactive oxygen species (ROS), we hypothesize myocyte damage and LV dysfunction are mediated by mitochondrially produced ROS and can be attenuated by the mitochondrially targeted antioxidant, mitoubiquinone (MitoQ). Methods: Aortocaval fistula (ACF) was induced for 8 weeks in adult rats ± MitoQ. Echocardiography and high-fidelity LV pressure catheter recordings were used to study the LV end-systolic pressure-volume relationship and cardiac efficiency. Isolated cardiomyocytes were loaded with Carboxy-H2DFFDA (CM-DCF) and tetramethylrhodamine (TMRM) to measure mitochondrial ROS production and membrane potential. Results: Isolated cardiomyocyte studies demonstrated increased ROS production and decreased mitochondrial membrane potential in VO animals, both of which were attenuated with MitoQ. Treatment with MitoQ demonstrated a strong trend toward improvement in LV contractility, as cardiac efficiency improved significantly in MitoQ-treated VO animals. Untreated VO animals exhibited mitochondrial swelling and myofibrillar disruption that was prevented by MitoQ. Conclusion: These studies suggest an early interplay between mitochondrial-derived ROS production and cardiac ultrastructure and function.

Cardiac efficiency

1995 ◽  
Vol 30 (5) ◽  
pp. 627-634 ◽  
Author(s):  
C Gibbs
Keyword(s):  
Cardiac Efficiency

The effects of aerobic fitness and β1-adrenergic receptor blockade on cardiac work during dynamic exercise

2009 ◽  
Vol 106 (2) ◽  
pp. 486-493 ◽  
Author(s):  
Megan N. Hawkins ◽  
Quinton Barnes ◽  
Sushmita Purkayastha ◽  
Wendy Eubank ◽  
Shigehiko Ogoh ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Stroke Volume ◽  
Systolic Blood Pressure ◽  
Adrenergic Receptor ◽  
Moderate Intensity ◽  
Receptor Blockade ◽  
Cardiac Efficiency ◽  
Cardiac Work ◽  
Total Body Oxygen ◽  
Adrenergic Receptor Blockade

The purpose of this investigation was to determine whether cardiovascular adaptations characteristic of long-term endurance exercise compensate more effectively during cardioselective β1-adrenergic receptor blockade-induced reductions in sympathoadrenergic-stimulated contractility. Endurance-trained (ET) athletes ( n = 8) and average-trained (AT; n = 8) subjects performed submaximal cycling exercise at moderate [45% maximum oxygen uptake (V̇o2max)] and heavy (70% V̇o2max) workloads, with and without metoprolol. Cardiac output (Q̇c), heart rate (HR), and systolic blood pressure were recorded at rest and during exercise. Cardiac work was calculated from the triple product of HR, stroke volume, and systolic blood pressure, and myocardial efficiency is represented as cardiac work for a given total body oxygen consumption. Metoprolol reduced Q̇c at 45% V̇o2max ( P = 0.004) and 70% V̇o2max ( P = 0.022) in ET subjects, but did not alter Q̇c in the AT subjects. In ET subjects at 45% V̇o2max, metoprolol-induced reductions in Q̇c were a result of decreases in HR ( P < 0.05) and the absence of a compensatory increase in stroke volume ( P > 0.05). The cardiac work and calculated cardiac efficiency were reduced with metoprolol in ET subjects at both exercise intensities and in the AT subjects during the high-intensity workload ( P < 0.01). The cardiac work and the calculated cardiac efficiency were not affected by metoprolol in the AT subjects during the 45% V̇o2max exercise. Therefore, in AT subjects, β-blockade reduced the amount of pressure generation necessary to produce the same amount of work during moderate-intensity exercise. In patients with heart disease receiving metoprolol, a decrease in the generation of cardiac pressure necessary to perform a given amount of work during mild-to-moderate exercise would prove to be beneficial.

One-day cold perfusion of bimakalim and butanedione monoxime restores ex situ cardiac function

1996 ◽  
Vol 271 (5) ◽  
pp. H1884-H1892 ◽  
Author(s):  
D. F. Stowe ◽  
B. M. Graf ◽  
S. Fujita ◽  
G. J. Gross
Keyword(s):  
Cardiac Function ◽  
Myocardial Function ◽  
Left Ventricular Pressure ◽  
Katp Channels ◽  
Left Ventricular ◽  
Ex Situ ◽  
Control Group ◽  
Cardiac Efficiency ◽  
Time Control ◽  
Butanedione Monoxime

Bimakalim (Bim), an opener of ATP-sensitive K+ (KATP) channels, was given alone or with 2,3-butanedione monoxime (BDM), a reversible uncoupler of contractility, to protect myocardial function during 1 day of hypothermia. Left ventricular pressure (LVP), coronary flow (CF), percent O2 extraction (%O2E), and cardiac efficiency were measured in 96 isolated, perfused guinea pig hearts divided into seven groups: 1) cold control (no drugs); 2) BDM; 3) Bim; 4) BDM + Bim; 5) BDM + glibenclamide (Glib, a blocker of KATP channels); 6) BDM + Bim + Glib; and 7) time control (6 h warm perfusion only). Drugs were given before, during, and initially after 22 h of low CF at 3.8 degrees C. At 26 h (cold groups) or 4 h (warm group) LVP (mmHg; means +/- SE) was similar for time control (94 +/- 4) and BDM + Bim (92 +/- 4) groups, lower and equivalent in the BDM (65 +/- 7) and BDM + Bim + Glib (64 +/- 7) groups, but LVP was higher than in the Bim group (46 +/- 3), and lowest in the cold control (30 +/- 8) group. In addition, only in the BDM + Bim group were basal CF, %O2E, and cardiac efficiency returned to values obtained in the time control group. Epinephrine increased LVP to that of the time control (106 +/- 3) group only in the BDM + Bim group (106 +/- 3) after hypothermia, and CF increases with adenosine, 5-hydroxytryptamine, and nitroprusside were similar to that of the time control group only in the BDM + Bim group after hypothermia. All of the effects of Bim were reversed by Glib. These results indicate that Bim, given with BDM, effectively preserves myocardial function and metabolism as well as inotropic and vasodilatory reserve during long-term hypothermic preservation as if the 1-day hypothermic state had not been instituted. Because the beneficial effects of Bim are blocked by Glib, the protective effect of Bim likely results from maintained KATP channel opening. Treatment with exogenous KATP openers may prove useful in preserving cardiac function in the transplanted heart.

Proinflammatory cytokines depress cardiac efficiency by a nitric oxide-dependent mechanism

1998 ◽  
Vol 275 (3) ◽  
pp. H1016-H1023 ◽  
Author(s):  
Donna Panas ◽  
Fadi H. Khadour ◽  
Csaba Szabó ◽  
Richard Schulz
Keyword(s):  
Nitric Oxide ◽  
Proinflammatory Cytokines ◽  
Heart Function ◽  
Early Response ◽  
Interferon Γ ◽  
Cardiac Efficiency ◽  
Cardiac Work ◽  
Rat Hearts ◽  
Inos Inhibitor ◽  
Factor Α

Proinflammatory cytokines (interleukin-1β, tumor necrosis factor-α, and interferon-γ; Cytomix) depress myocardial contractile work partially by stimulating expression of inducible nitric oxide (NO) synthase (iNOS). Because NO and peroxynitrite inhibit myocardial O2 consumption (MV˙o 2), we examined whether this mechanism contributes to reduced cardiac work. In control isolated working rat hearts, cardiac work was stable for 60 min, followed by a decline from 60 to 120 min, without change in MV˙o 2. Cardiac efficiency (work/MV˙o 2) was therefore reduced from 60 to 120 min. Cytomix shortened the onset (within 20–40 min) and enhanced the depression in cardiac work and efficiency and inhibited MV˙o 2 after 80 min. Mercaptoethylguanidine (MEG), an iNOS inhibitor and peroxynitrite scavenger, or the glucocorticoid dexamethasone (Dex) abolished the effects of Cytomix. iNOS expression was increased 10-fold by Cytomix and abolished by Dex but not MEG. That cytokine-induced depression in cardiac work precedes the reduction in MV˙o 2 suggests, at least in the early response, that NO and/or peroxynitrite may not impair heart function by inhibiting mitochondrial respiration but reduce the heart’s ability to utilize ATP for contractile work.

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