Inotropic augmentation of myocardial oxygen consumption

Clancy, R. L.; Tp, Graham; Wj, Powell; Jp, Gilmore

doi:10.1152/ajplegacy.1967.212.5.1055

Cited by 45 publications

(9 citation statements)

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“…Moreover, the increase in MVos with increased contractility occurred under conditions in which peak developed tension and contractile element work remained constant, and total developed tension actually decreased. These results serve to quantify and to place into perspective previous investigations showing increases in MVo2 with increases in contractility produced by sympathetic nerve stimulation or excitement (13), isoproterenol (14), norepinephrine (15,17), cardiac glycosides (16)(17)(18), Ca++ (15), and paired electrical stimulation (15). It has also been reported that increases in contractility produced by cardiac glycosides (26), norepinephrine (27), and Ca++ (28) do not always augment MVo2.…”

Section: Resultsmentioning

confidence: 56%

“…This effect has been demonstrated both for positive inotropic interventions, which increase MVo2 when myocardial tension is held constant or falls (13)(14)(15)(16)(17)(18), and also for negative inotropic interventions which reduce MVo2 at constant levels of tension (11). It has been suggested that this effect of the contractile or inotropic state on MVo2 might be related to changes in (a) the velocity of shortening of the contractile elements (CE) and myocardial fibers, (b) the extent of shortening of the CE and of the myocardial fibers, and (c) the contractile state as reflected in the extrapolated velocity of shortening of the unloaded CE (Vmax).…”

Section: Introductionmentioning

confidence: 88%

“…Recently, it has also become apparent that wall tension is not the' sole determinant of the heart's oxygen utilization, and there is' substantial evidence that changes in myocardial contractility, or inotropic state, as reflected in Vmax, the maximum velocity of shortening of the unloaded-contractile elements, can exert considerable influence on MVo2 (11,(13)(14)(15)(16)(17)(18). This effect has been demonstrated both for positive inotropic interventions, which increase MVo2 when myocardial tension is held constant or falls (13)(14)(15)(16)(17)(18), and also for negative inotropic interventions which reduce MVo2 at constant levels of tension (11).…”

Section: Introductionmentioning

confidence: 99%

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Control of myocardial oxygen consumption: relative influence of contractile state and tension development

Graham¹,

Covell²,

Sonnenblick³

et al. 1968

J. Clin. Invest.

261

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A B S T R A C T Myocardial oxygen consumption was measured in 11 anesthetized, open-chest dogs in order to compare in the same heart the relative influence on oxygen usage of tension development and the contractile or inotropic state, as reflected in Vmax, the maximum velocity of shortening of the unloaded contractile elements. The isovolumetrically contracting left ventricle was studied with left ventricular volume, heart rate, and systemic perfusion rate controlled. Wall tension, contractile element velocity, and Vmax were calculated. Peak developed tension was increased at a constant Vma. by increasing ventricular volume, and the effect Onl oxygen consumption was determined. Oxygen utilization was then redetermined at an increased Vmax but at a constant peak developed tension by infusing norepinephrine (0.76 to 7.6 jug/min) and decreasing ventricular volume to match the tension existing before norepinephrine infusion. Oxygen consumption consistently increased with increases in both developed tension and VnaX With the following multiple regression equation relating these variables: myocardial oxygen consumption (dl/beat per 100 g in LV) = K + 0.25 peak developed tension (g/cm2) + 1.43 Vmx,,, (cm/sec). These data indicate that the oxygen cost of augmentation of contractility is sub-

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Section: Resultsmentioning

confidence: 56%

Section: Introductionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Control of myocardial oxygen consumption: relative influence of contractile state and tension development

Graham¹,

Covell²,

Sonnenblick³

et al. 1968

J. Clin. Invest.

261

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show abstract

“…Ventricular contractility, as assessed by developed wall tension and the rate of contractile element shortening, has been shown to be an important determinant of MVo 2 and coronary vascular resistance (2,3). The converse causal relationship (viz., coronary blood flow as a determinant of contractility), however, has not been established.…”

mentioning

confidence: 99%

“…Changes in the contractile state were assessed by comparisons of the maximum measured velocity (max V ce ) (15,18). The force at which comparisons were made for each individual animal was the lowest force common to all curves 2 By assuming a left ventricular spherical model rather than a prolate spheroid of identical volume (major-minor axis of 2:1), the base-to-apex fiber length is equal to the circumferential diameter. The relative error between the two systems of calculating force is 8% (16).…”

mentioning

confidence: 99%

Effects of Coronary Blood Flow and Perfusion Pressure on Left Ventricular Contractility in Dogs

Abel

Reis

1970

Circulation Research

101

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The effects of changes in coronary blood flow and coronary artery pressure on left ventricular (LV) contractility were determined in 18 animals. Dogs on cardiopulmonary bypass provided isovolumetric LV contractions during controlled perfusion of the coronary circulation. Coronary venous efflux, myocardial oxygen consumption, peak LV pressure, LV dp/dt, and the forcevelocity relations of the LV were determined at normal and at "supernormal" levels of flow and pressure. Coronary vasodilatation was obtained with nitroglycerine, permitting independent variation of flow and pressure. Augmenting flow by increasing pressure increased LV contractility, as reflected by increases in peak LV pressure, dp/dt max, peak wall tension, and maximal measured contractile element velocity. Increased contractility appeared to be primarily due to increased flow, rather than to pressure, as an increase in flow without an increase in pressure produced similar changes, and decreases in pressure at constant flow did not change maximal measured contractile element velocity or dp/dt max, although some decrease in peak LV pressure and wall tension did occur. These data suggest that coronary flow is an independent determinant of the contractile state of myocardium, and that an increase in flow in excess of that required to supply metabolic demands augments myocardial contractility. ADDITIONAL KEY WORDSmyocardial contractility nitroglycerine coronary vascular resistance myocardial oxygen consumption contractile element velocity force-velocity relations inotropic state ventricular compliance• The relationships between ventricular work, coronary blood flow and myocardial oxygen consumption (MVo 2 ) are well established (1). Ventricular contractility, as assessed by developed wall tension and the rate of contractile element shortening, has been shown to be an important determinant of MVo 2 and coronary vascular resistance (2, 3). The converse causal relationship (viz., coronary blood flow as a determinant of contractility), however, has not been established. Gregg (4, 5) observed that a change in left circumflex artery perfusion pressure caused directional changes in both coronary flow and MV02 without consistent changes in heartFrom the Clinic of Surgery, National Heart and Lung Institute, Bethesda, Maryland 20014.Received April 2, 1970; accepted for publication October 19, 1970. rate, cardiac output, aortic pressure, or left ventricular end-diastolic pressure (LV, EDP). "Gregg's phenomenon" or the suggestion that coronary flow and coronary artery pressure (CAP) were independent determinants of MV02 and ventricular contractility has been investigated in several laboratories by a variety of experimental methods (6-9). The results of these studies have been the subject of controversy possibly related to the variety of preparations utilized, amount of myocardial work generated in these studies and the failure to differentiate between the effects produced by changes in coronary flow versus coronary artery pressure. The present studies we...

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Dobutamine Therapy in Acute Myocardial Infarction

Keung¹

1981

JAMA

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The short-term response of combined dopamine hydrochloride-sodium nitroprusside therapy was compared with administration of dobutamine in eight patients with acute myocardial infarction complicated by hypotension and severe left ventricular dysfunction. All patients were receiving dopamine before the study began. The addition of sodium nitroprusside increased cardiac index (Cl) from 1.94 +/- 0.490 to 2.22 +/- 0.48 L/min/sq m; decreased left ventricular filling pressure (LVFP) from 28.9 +/- 3.5 to 19.9 +/- 3.3 mm Hg and mean systemic arterial pressure (MAP) from 82.1 +/- 5.1 to 71.5 +/- 6.0 mm Hg. During dobutamine infusion, Cl, LVFP, and MAP were 2.33 +/- 0.31 L/min/sq m, 20.8 +/- 4.8 mm Hg, and 74.1 +/- 8.1 mm Hg, respectively. There was no statistical difference between short-term hemodynamic benefits produced by dobutamine or combined dopamine-sodium nitroprusside therapy. Dobutamine, a synthetic cathecholamine, provides a substitute for dopamine-sodium nitroprusside therapy in acute myocardial infarction. Dobutamine has the advantage of being a single agent and is therefore easier to administer.

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Inotropic augmentation of myocardial oxygen consumption

Cited by 45 publications

References 0 publications

Control of myocardial oxygen consumption: relative influence of contractile state and tension development

Control of myocardial oxygen consumption: relative influence of contractile state and tension development

Effects of Coronary Blood Flow and Perfusion Pressure on Left Ventricular Contractility in Dogs

Dobutamine Therapy in Acute Myocardial Infarction

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