Myocardial oxygen consumption, cardiac work, and myocardial efficiency in children

1996 ◽  
Vol 155 (6) ◽  
pp. 436-439 ◽  
Author(s):  
Zenshiro Onouchi ◽  
Kenji Hamaoka ◽  
Koichi Sakata ◽  
Yali Liu ◽  
Fumiaki Suto ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Myocardial Oxygen Consumption ◽  
Cardiac Work ◽  
Myocardial Efficiency

Coupled pacing improves cardiac efficiency during acute atrial fibrillation with or without cardiac dysfunction

2004 ◽  
Vol 287 (5) ◽  
pp. H2016-H2022 ◽  
Author(s):  
Hirotsugu Yamada ◽  
Kent A. Mowrey ◽  
Zoran B. Popović ◽  
William J. Kowalewski ◽  
David O. Martin ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Oxygen Consumption ◽  
Energy Consumption ◽  
Cardiac Dysfunction ◽  
Myocardial Oxygen Consumption ◽  
Ventricular Rate ◽  
Cardiac Work ◽  
Paired Stimulation ◽  
Myocardial Efficiency

Coupled pacing (CP), a method for controlling ventricular rate during atrial fibrillation (AF), consists of a single electrical stimulation applied to the ventricles after each spontaneous activation. CP results in a mechanical contraction rate approximately one-half the rate during AF. Paired stimulation in which two electrical stimuli are delivered to the ventricles has also been proposed as a therapy for heart failure. Although paired stimulation enhances contractility, it greatly increases energy consumption. The primary hypothesis of the present study is that CP improves cardiac function during acute AF without a similar increase in energy consumption because of the reduced rate of ventricular contractions. In a canine model, CP was applied during four stages: sinus rhythm (SR), acute AF, cardiac dysfunction (CD), and AF in the presence of cardiac dysfunction. The rate of ventricular contraction decreased in all four stages as the result of CP. In addition, we determined the changes in external cardiac work, myocardial oxygen consumption, and myocardial efficiency in the each of four stages. CP partially reversed the effects of AF and CD on external cardiac work, whereas myocardial oxygen consumption increased only moderately. In all stages but SR, CP increased myocardial efficiency because of the marked increases in cardiac work compared with the moderate increases in total energy consumed. Thus this pacing therapy may be a viable therapy for patients with concurrent atrial fibrillation and heart failure.

Effect of work on intracellular calcium of the intact heart

1991 ◽  
Vol 261 (4) ◽  
pp. 54-59
Author(s):  
Teresa A. Fralix ◽  
Frederick W. Heineman ◽  
Robert S. Balaban
Keyword(s):  
Oxygen Consumption ◽  
Oxidative Phosphorylation ◽  
Intracellular Calcium ◽  
Myocardial Oxygen Consumption ◽  
Contractile Activity ◽  
Rabbit Heart ◽  
Metabolic Process ◽  
Contractile Apparatus ◽  
Cardiac Work ◽  
Intact Heart

Intracellular calcium has been proposed to play a key role in the orchestration of metabolic rate with contractile activity in the mammalian heart. Calcium is believed to accomplish this task by modulating the contractile apparatus as well as the metabolic process directly, and perhaps simultaneously, during alterations in cardiac work. The purpose of this study was to evaluate whether appropriate changes in intracellular calcium accompany alterations in cardiac work in the intact working rabbit heart. A range of myocardial oxygen consumption was obtained from 0.94 to 6.51 μmol·g LV wt-1·min-1 by changing afterload or -agonist addition. With the increase in work and associated increase in respiration, an increase in intracellular calcium was observed, on the basis of indo-1 fluorescence. These results indicate that intracellular calcium is a valid candidate as a cytosolic transducer contributing to the orchestration of myofibril adenosinetriphosphatase activity and oxidative phosphorylation in the intact heart. oxygen consumption; indo-1; fluorescence; rabbit; afterload; isoproterenol

Effect of work on intracellular calcium of the intact heart

1991 ◽  
Vol 261 (4) ◽  
pp. L54-L59
Author(s):  
Teresa A. Fralix ◽  
Frederick W. Heineman ◽  
Robert S. Balaban
Keyword(s):  
Oxygen Consumption ◽  
Intracellular Calcium ◽  
Myocardial Oxygen Consumption ◽  
Contractile Activity ◽  
Rabbit Heart ◽  
Metabolic Process ◽  
Beta Agonist ◽  
Contractile Apparatus ◽  
Cardiac Work ◽  
Intact Heart

Intracellular calcium has been proposed to play a key role in the orchestration of metabolic rate with contractile activity in the mammalian heart. Calcium is believed to accomplish this task by modulating the contractile apparatus as well as the metabolic process directly, and perhaps simultaneously, during alterations in cardiac work. The purpose of this study was to evaluate whether appropriate changes in intracellular calcium accompany alterations in cardiac work in the intact working rabbit heart. A range of myocardial oxygen consumption was obtained from 0.94 to 6.51 μmol·g LV wt-1·min-1 by changing afterload or beta-agonist addition. With the increase in work and associated increase in respiration, an increase in intracellular calcium was observed, on the basis of indo-1 fluorescence. These results indicate that intracellular calcium is a valid candidate as a cytosolic transducer contributing to the orchestration of myofibril adenosinetriphosphatase activity and oxidative phosphorylation in the intact heart. oxygen consumption; indo-1; fluorescence; rabbit; afterload; isoproterenol

scholarly journals Levosimendan improves cardiac function and myocardial efficiency in rats with right ventricular failure

2017 ◽  
Vol 8 (1) ◽  
pp. 204589321774312 ◽  
Author(s):  
Mona S. Hansen ◽  
Asger Andersen ◽  
Lars P. Tolbod ◽  
Nils H. Hansson ◽  
Roni Nielsen ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Cardiac Function ◽  
Right Ventricular ◽  
Glucose Uptake ◽  
Myocardial Oxygen Consumption ◽  
External Work ◽  
Myocardial Glucose Uptake ◽  
Positron Emission ◽  
Myocardial Efficiency ◽  
Rv Function

Levosimendan is an inotropic and vasodilator drug, which is known to improve cardiac function in animal models of right ventricular (RV) failure. The effects of levosimendan on oxygen consumption and myocardial efficiency in the failing RV is unknown. We investigated the effects of levosimendan on RV function, myocardial oxygen consumption, myocardial external efficiency (MEE), and myocardial metabolism in rats with RV hypertrophy and failure. RV hypertrophy and failure were induced by pulmonary trunk banding in rats. Rats were randomized to seven weeks of treatment with vehicle (n = 16) or levosimendan (3 mg/kg/day) (n = 13). Control animals without pulmonary banding received vehicle treatment (n = 11). RV MEE and RV metabolism were evaluated by echocardiography, 11C-acetate positron emission tomography (PET), 18F-FDG PET, and invasive pressure measurements. We found that levosimendan improved RV MEE (26 ± 3 vs. 14 ± 1%, P < 0.01) by increasing RV external work (0.62 ± 0.06 vs. 0.30 ± 0.03 mmHgċmL, P < 0.001) without affecting RV myocardial oxygen consumption ( P = 0.64). The improvement in RV MEE was not associated with a change in RV myocardial glucose uptake (1.3 ± 0.1 vs. 1.0 ± 0.1 µmol/g/min, P = 0.44). In conclusion, in the hypertrophic and failing RV of the rat, levosimendan improves RV function without increasing myocardial oxygen consumption leading to improved MEE. The improvement in RV MEE was not associated with a change in myocardial glucose uptake. This study emphasizes the potential therapeutic value of chronic levosimendan treatment RV failure. It extends previous observations on the effect profile of levosimendan and motivates clinical testing of levosimendan in RV failure.

Effect of hyperosmotic mannitol on myocardial oxygen consumption

1977 ◽  
Vol 233 (4) ◽  
pp. H444-H450
Author(s):  
G. J. Vlahakes ◽  
W. J. Powell
Keyword(s):  
Oxygen Consumption ◽  
Myocardial Oxygen Consumption ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Tension Time ◽  
Anesthetized Dogs ◽  
Myocardial Efficiency ◽  
Experimental Myocardial Ischemia

Hyperosmotic mannitol produces salutary hemodynamic and histologic effects during experimental myocardial ischemia. However, the administration of hyperosmotic mannitol is associated with a positive inotropic influence. Positive inotropic interventions, which increase myocardial oxygen consumption (MVO2), also tend to increase the extent of ischemic myocardial injury. Thus, the purpose of this study was to determine the effect of mannitol on MVO2. Anesthetized dogs on right-heart bypass under conditions of controlled hemodynamics were studied. Both coronary arteries were perfused; mannitol was infused via the coronary perfusion cannulas to produce a 35 mosmol increase in osmolality. Heart rate was maintained constant. Cardiac output was held constant or deliberately increased so that left ventricular end-diastolic pressure and tension-time index, two other hemodynamic correlates of MVO2, remained constant or increased. MVO2 significantly decreased under conditions of decreased myocardial perfusion (P less than 0.025). This was in spite of a significant increase (P less than 0.001) in the peak rate of rise of left ventricular pressure (LV dP/dt), a hemodynamic correlate of MVO2. Thus, hyperosmotic mannitol under conditions of reduced coronary perfusion increases myocardial efficiency.

Effects of dipyridamole on myocardial adenosine and active hyperemia

1984 ◽  
Vol 247 (5) ◽  
pp. H804-H810 ◽  
Author(s):  
R. M. Knabb ◽  
J. M. Gidday ◽  
S. W. Ely ◽  
R. Rubio ◽  
R. M. Berne
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Steady State ◽  
Myocardial Oxygen Consumption ◽  
Cardiac Work ◽  
Adenosine Release ◽  
Adenosine Uptake ◽  
Adenosine Concentration ◽  
The Relationship ◽  
Perfused Hearts

Dipyridamole, a vasodilator that potentiates the actions of exogenous adenosine, is known to inhibit cellular uptake of adenosine, but its effects on cellular adenosine release, and thus interstitial adenosine levels, are disputed. We used the accumulation of adenosine in pericardial infusates (PCI) as an index of interstitial adenosine concentration and observed the effects of dipyridamole on relationships among coronary blood flow (CBF), myocardial oxygen consumption (MVO2), and PCI adenosine concentrations during steady-state alterations of cardiac work. Dipyridamole increased CBF and PCI adenosine concentration without altering MVO2. The relationship between PCI adenosine and CBF was unaltered, supporting a cause and effect relationship between interstitial adenosine concentration and CBF. In addition, we determined that unlike previous studies in isolated perfused hearts the washout of adenosine by coronary plasma was unaffected by dipyridamole. The results support previous suggestions that, whereas dipyridamole inhibits adenosine uptake, it does not alter cellular adenosine release, and therefore interstitial adenosine levels are increased. The constant relationship between PCI adenosine and CBF supports hypotheses that attribute the hyperemias associated with increased cardiac work or with dipyridamole to increased interstitial adenosine.

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