Consistent substrate utilization despite reduced flow in hearts with maintained work

1983 ◽  
Vol 244 (6) ◽  
pp. H799-H806 ◽  
Author(s):  
K. A. Fox ◽  
H. Nomura ◽  
B. E. Sobel ◽  
S. R. Bergmann
Keyword(s):  
Heart Rate ◽  
Oxygen Consumption ◽  
Myocardial Oxygen Consumption ◽  
Myocardial Metabolism ◽  
Diastolic Pressure ◽  
Rabbit Heart ◽  
Substrate Utilization ◽  
Left Ventricular ◽  
Low Flow ◽  
Heart Preparation

Assessments of myocardial metabolism based on external detection of accumulation of radiolabeled substrates may be influenced, as a result of alterations in flow, by altered substrate delivery as well as altered work (with concomitant changes in metabolic requirements). To determine whether reduced delivery limits substrate utilization under defined conditions of reduced perfusion, an isolated rabbit heart preparation was employed in which flow was reduced but myocardial oxygen consumption (MVo2) and work were kept constant by adjustment of left ventricular end-diastolic pressure and heart rate. Flow was reduced from 1.5 to 0.5 ml . g-1 . min-1, while work was maintained constant in hearts functioning at either low or high levels of MVo2. Consumption of palmitate remained constant (48.8 +/- 11.6 and 68.8 +/- 23.3 nmol . g-1 . min-1), because the proportion of palmitate extracted increased (8.8 +/- 4 to 29.1 +/- 7.2% and 10.3 +/- 3.4 to 21.0 +/- 6.1%). The results indicate that, despite reduction of flow, hearts at constant work loads can extract increasing proportions of delivered substrates such that net utilization remains constant until flow is reduced below the level required to maintain cellular function. They suggest that, under conditions of low flow, impaired extraction of substrates reflects either primarily or secondarily depressed myocardial metabolism rather than simply decreased delivery of substrate.

Alteration in myocardial oxygen balance during exercise after beta-adrenergic blockade in dogs

1980 ◽  
Vol 49 (1) ◽  
pp. 28-33 ◽  
Author(s):  
G. R. Heyndrickx ◽  
J. L. Pannier ◽  
P. Muylaert ◽  
C. Mabilde ◽  
I. Leusen
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Myocardial Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Myocardial Oxygen Consumption ◽  
Left Ventricular ◽  
Adrenergic Blockade ◽  
Oxygen Balance

The effects of beta-adrenergic blockade upon myocardial blood flow and oxygen balance during exercise were evaluated in eight conscious dogs, instrumented for chronic measurements of coronary blood flow, left ventricular pressure, aortic blood pressure, heart rate, and sampling of arterial and coronary sinus venous blood. The administration of propranolol (1.5 mg/kg iv) produced a decrease in heart rate, peak left ventricular (LV) dP/dt, LV (dP/dt/P, and an increase in LV end-diastolic pressure during exercise. Mean coronary blood flow and myocardial oxygen consumption were lower after propranolol than at the same exercise intensity in control conditions. The oxygen delivery-to-oxygen consumption ratio and the coronary sinus oxygen content were also significantly lower. It is concluded that the relationship between myocardial oxygen supply and demand is modified during exercise after propranolol, so that a given level of myocardial oxygen consumption is achieved with a proportionally lower myocardial blood flow and a higher oxygen extraction.

Negative inotropism of hyperthermia increases oxygen cost of contractility in canine hearts

2000 ◽  
Vol 279 (6) ◽  
pp. H2855-H2864 ◽  
Author(s):  
Akio Saeki ◽  
Yoichi Goto ◽  
Katsuya Hata ◽  
Toshiyuki Takasago ◽  
Takehiko Nishioka ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Baseline Level ◽  
Myocardial Oxygen Consumption ◽  
Myocardial Metabolism ◽  
Mechanical Energy ◽  
Left Ventricular ◽  
Lv Function ◽  
Oxygen Cost ◽  
Negative Inotropism ◽  
Total Mechanical Energy

Heart temperature affects left ventricular (LV) function and myocardial metabolism. However, how and whether increasing heart temperature affects LV mechanoenergetics remain unclear. We designed the present study to investigate effects of increased temperature by 5°C from 36°C on LV contractility and energetics. We analyzed the LV contractility index ( Emax) and the relation between the myocardial oxygen consumption (MV˙o2) and the pressure-volume area (PVA; a measure of LV total mechanical energy) in isovolumically contracting isolated canine hearts during normothermia (NT) and hyperthermia (HT). HT reduced Emaxby 38% ( P < 0.01) and shortened time to Emaxby 20% ( P < 0.05). HT, however, altered neither the slope nor the unloaded MV˙o2of the MV˙o2-PVA relation. HT increased the oxygen cost of contractility (the incremental ratio of unloaded MV˙o2to Emax) by 49%. When Ca2+infusion restored the reduced LV contractility during HT to the NT baseline level, the unloaded MV˙o2in HT exceeded the NT value by 36%. We conclude that HT-induced negative inotropism accompanies an increase in the oxygen cost of contractility.

Myocardial contracture and accumulation of mitochondrial calcium in ischemic rabbit heart

1977 ◽  
Vol 233 (6) ◽  
pp. H677-H684 ◽  
Author(s):  
P. D. Henry ◽  
R. Schuchleib ◽  
J. Davis ◽  
E. S. Weiss ◽  
B. E. Sobel
Keyword(s):  
Intracellular Calcium ◽  
Diastolic Pressure ◽  
Mitochondrial Fraction ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Low Flow ◽  
Mitochondrial Calcium ◽  
Close Relationship ◽  
Diastolic Relaxation ◽  
Mechanical Recovery

The relationship between myocardial contracture and cell calcium was studied in electrically paced, isolated perfused rabbit hearts. Isovolumic left ventricular dP/dt and end-diastolic pressure were utilized as indexes of contractility and ventricular stiffness. After 60 min of low flow (ischemia) without or with reperfusion at high flow for 10 min, calcium was measured in the mitochondrial fraction and used as an indicator of intracellular calcium. Low flow led to ventricular standstill and contracture, and reperfusion produced partial mechanical recovery with end-diastolic pressure remaining markedly elevated. Nifedipine (10(-7) M), an antagonist of myocardial calcium uptake, prevented contracture and permitted nearly complete mechanical recovery without elevation in diastolic pressure. Increases in mitochondrial calcium paralleled the severity of contracture and the lack of diastolic relaxation after reperfusion. Mitochondrial calcium did not increase in hearts protected by nifedipine. Results demonstrate a close relationship between mechanical changes induced by ischemia and accumulation of intracellular calcium.

Left ventricular heat production during induced tachycardia in the intact dog

1965 ◽  
Vol 209 (1) ◽  
pp. 33-36 ◽  
Author(s):  
Skoda Afonso ◽  
David H. McKenna ◽  
George S. O'Brien ◽  
George G. Rowe ◽  
Charles W. Crumpton
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Metabolic Rate ◽  
Coronary Blood Flow ◽  
Heat Production ◽  
Myocardial Oxygen Consumption ◽  
Left Ventricular ◽  
Metabolic Parameters ◽  
Heat Control

It is well established that heart rate is a determinant of myocardial oxygen consumption. However, it has not been demonstrated that the increase of oxygen consumption at faster rates actually represents loss of energy, degraded as heat. Control measurements of systemic and coronary hemodynamic and metabolic parameters and left ventricular heat production (measured by a recently reported method) were obtained in 10 dogs. Tachycardia was then induced electrically and the same parameters redetermined. Significant increases occurred in coronary blood flow, cardiac metabolic rate of oxygen, and left ventricular heat production. The elevated myocardial oxygen consumption at higher rates is associated with increased heat production.

Effects of Intraduodenal Administration of "Kyushin," a Senso (Toad Venom)-Containing Drug, on Systemic Hemodynamics, CardiacFunction and Myocardial Oxygen Consumption in Anesthetized Dogs

1993 ◽  
Vol 21 (01) ◽  
pp. 7-16 ◽  
Author(s):  
Matao Sakanashi ◽  
Katsuhiko Noguchi ◽  
Takao Chibana ◽  
Yoshihiko Ojiri ◽  
Masamichi Shoji
Keyword(s):  
Oxygen Consumption ◽  
Myocardial Oxygen Consumption ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Cardiovascular Effects ◽  
Left Ventricular ◽  
Toad Venom ◽  
The Relationship ◽  
Cardiotonic Effect ◽  
Intraduodenal Administration

The effects of "Kyushin" (KY), a Senso (toad venom)-containing drug, on the cardiovascular system were examined by intraduodenal administration of KY in anesthetized open-chest dogs. KY (3 or 10 mg/kg) dose-dependently increased the peak positive first derivative of left ventricular pressure ((+)LVdP/dt) and mean aortic pressure, and decreased the left ventricular end-diastolic pressure (LVEDP). Myocardial oxygen consumption (MVO2) and heart rate (HR) were not significantly influenced by KY. KY produced a cardiotonic effect without any increase in MVO2, because the increase in MVO2 due to the cardiotonic effect of KY may have been cancelled by a decrease in MVO2 due to reduction of preload and the lack of increase in HR. In order to clarify the relationship between the cardiovascular effects of KY and the drug concentration in plasma, the concentration of anti-bufalin IgG reactive substance (BRS) in plasma was measured by enzyme immunoassay. The maximum BRS concentrations 20 min after administration of 3 and 10 mg/kg KY were dose-dependent. From the relationship between changes in (+)LVdP/dt and changes in BRS concentration after administration of KY, it is inferred that the effective concentration of BRS in plasma at which KY produces a cardiotonic effect in dogs is approximately 2-3 ng/ml.

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.

Measurement of the activation time of oxidative phosphorylation in isolated mouse hearts

2000 ◽  
Vol 279 (6) ◽  
pp. H3118-H3123 ◽  
Author(s):  
Lori A. Gustafson ◽  
Johannes H. G. M. Van Beek
Keyword(s):  
Heart Rate ◽  
Oxygen Consumption ◽  
Oxidative Phosphorylation ◽  
Response Time ◽  
Myocardial Metabolism ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Rate Pressure Product ◽  
Activation Time ◽  
Dynamic Regulation

The purpose of this study was to develop a technique for determination of the dynamic regulation of oxidative myocardial metabolism in the mouse. The response time of myocardial oxygen consumption (MV˙o 2) to a step in heart rate was determined in Langendorff-perfused mouse hearts. We examined the effect of glucose-only perfusate and glucose combined with 1, 3, or 6 mM pyruvate. Left ventricular systolic pressure (LVSP) decreased, yet the rate-pressure product (RPP) and MV˙o 2 increased with upward steps in heart rate. Pyruvate increased LVSP, RPP, and MV˙o 2 at the lower concentrations; however, when 6 mM pyruvate was added, LVSP and RPP became depressed while MV˙o 2 remained elevated. The mean response time of oxygen consumption to a step in heart rate from 270 to 350 beats/min was 9.8 s ( n = 7) in the glucose-only perfused hearts. Perfusion with glucose plus 6 mM pyruvate decreased the response time to 5.3 s. These results are similar to those found in the rabbit heart and lay the groundwork for further examination of the dynamic regulation of oxidative myocardial metabolism in genetically altered mice. We concluded that the activation time of oxidative phosphorylation in the mouse is similar to that in larger species, despite the high mitochondrial content and natural heart rate of the mouse.

Cardiac dysfunction in terms of left ventricular mechanical work and energetics in hypothyroid rats

2002 ◽  
Vol 283 (2) ◽  
pp. H631-H641 ◽  
Author(s):  
Yoshimi Ohga ◽  
Susumu Sakata ◽  
Chikako Takenaka ◽  
Takehisa Abe ◽  
Tsuyoshi Tsuji ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Cardiac Dysfunction ◽  
Myocardial Oxygen Consumption ◽  
Left Ventricular ◽  
Mechanical Work ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Plasmic Reticulum ◽  
Heart Preparation ◽  
Whole Heart

We hypothesized that cardiac dysfunction in hypothyroidism is mainly caused by the impairment of Ca2+ handling in excitation-contraction coupling. To prove this hypothesis, we investigated left ventricular (LV) mechanical work and energetics without interference of preload and afterload in an excised, blood-perfused whole heart preparation from hypothyroid rats. We found that LV inotropism and lusitropism were significantly depressed, and these depressions were causally related to decreased myocardial oxygen consumption for Ca2+ handling and for basal metabolism. The oxygen costs of LV contractility for Ca2+ and for dobutamine in the hypothyroid rats did not differ from those in age-matched normal rats. The expression of sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA2) significantly decreased and that of phospholamban significantly increased. The present results revealed that changes in LV energetics associated with decreased mechanical work in hypothyroid rats are mainly caused by the impairment of Ca2+ uptake via SERCA2. We conclude that the impairment of Ca2+ uptake plays an important role in the pathogenesis of cardiac dysfunction in hypothyroidism.

Clinical and Experimental Analysis of 201Thallium Uptake of the Heart

1978 ◽  
Vol 17 (04) ◽  
pp. 142-148
Author(s):  
U. Büll ◽  
S. Bürger ◽  
B. E. Strauer
Keyword(s):  
Oxygen Consumption ◽  
Left Ventricle ◽  
Muscle Mass ◽  
Myocardial Oxygen Consumption ◽  
Animal Experiments ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall ◽  
Flow Measurements ◽  
Myocardial Flow

Studies were carried out in order to determine the factors influencing myocardial 201T1 uptake. A total of 158 patients was examined with regard to both 201T1 uptake and the assessment of left ventricular and coronary function (e. g. quantitative ventriculography, coronary arteriography, coronary blood flow measurements). Moreover, 42 animal experiments (closed chest cat) were performed. The results demonstrate that:1) 201T1 uptake in the normal and hypertrophied human heart is linearly correlated with the muscle mass of the left ventricle (LVMM);2) 201T1 uptake is enhanced in the inner (subendocardial) layer and is decreased in the outer (subepicardial) layer of the left ventricular wall. The 201T1 uptake of the right ventricle is 40% lower in comparison to the left ventricle;3) the basic correlation between 201T1 uptake and LVMM is influenced by alterations of both myocardial flow and myocardial oxygen consumption; and4) inotropic interventions (isoproterenol, calcium, norepinephrine) as well as coronary dilatation (dipyridamole) may considerably augment 201T1 uptake in accordance with changes in myocardial oxygen consumption and/or myocardial flow.It is concluded that myocardial 201T1 uptake is determined by multiple factors. The major determinants have been shown to include (i) muscle mass, (ii) myocardial flow and (iii) myocardial oxygen consumption. The clinical data obtained from patient groups with normal ventricular function, with coronary artery disease, with left ventricular wall motion abnormalities and with different degree of left ventricular hypertrophy are correlated with quantitated myocardial 201T1 uptake.

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