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

Graham, T.P.; Covell, James W.; Sonnenblick, Edmund H.; Ross, John; Braunwald, Eugene

doi:10.1172/jci105734

Cited by 261 publications

(72 citation statements)

References 42 publications

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“…When arterial pressure in dogs was increased to levels at which autoregulation of coronary blood flow was lost (138±2 mm Hg), however, coronary flow reserve was reduced because resting coronary blood flow increased more than hyperemic coronary blood flow.39 Hence, although the results of our study in humans were similar to those performed in animals with an arterial pressure in the zone of coronary autoregulation, elevation of arterial pressure beyond the bounds of autoregulation might reduce maximal coronary reserve. In an open-chest, open-pericardium, anesthetized dog preparation in which coronary autoregulation was abolished with vasodilation (carbochromen or adenosine), increased left ventricular preload produced by volume expansion was associated with a reduction in the ratio of endocardial to epicardial coronary blood flow.4142 Total diastolic left circumflex coronary blood flow was either decreased41 or did not change.42 When heart rate and systemic perfusion rate were controlled in anesthetized, open-chest dogs, however, increased left ventricular volume was associated with increased left ventricular wall tension and myocardial oxygen demand. 43 Coronary blood flow increased in response to elevated left ventricular preload. The effect of increased left ventricular preload on total coronary blood flow in the conscious animal has not been studied.…”

Section: Previous Studiesmentioning

confidence: 99%

Interstudy variability of coronary flow reserve. Influence of heart rate, arterial pressure, and ventricular preload.

1990

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To define the long-term variability of serial coronary flow reserve (CFR) catheter and intracoronary papaverine. Initial CFR measurements were highly correlated with repeat measurements obtained 11±0.6 months later (r=0.95; mean absolute difference, 0.3±0.1; n=17). Differences in CFRbetween studies were related to changes in heart rate (r=0.61,p=0.01) but not to changes in mean arterial pressure (r=0.25, p=0.33). To define the effects of rapid changes in heart rate, mean arterial pressure, and preload on CFR, these variables were altered by atrial pacing, handgrip exercise, and volume expansion, respectively. Atrial pacing produced a rate-related increase in rCBFV but did not change hCBFV. Consequently, CFR was significantly reduced as heart rate was increased progressively from 76±2 in sinus rhythm (4.5+±0.2) to 100 (3.8±0.2, p<0.05, n=32) to 120 beats/min (3.2±0.1, p<0.05, n=7). Despite a 19±2 mm Hg rise in mean arterial pressure during handgrip exercise, CFR was unchanged from baseline (3.7±0.3 vs. 3.7±0.4, p=NS, n=7) because rCBFV rose proportionally with hCBFV. When pulmonary capillary wedge pressure was increased from 9±1 to 16±1 mm Hg after volume expansion, CFR was significantly decreased (from 3.8±0.2 to 2.9+±0.2, p<0.05, n=9) because rCBFV was increased while hCBFV remained unchanged. Hence, serial CFR measurements in humans are highly reproducible in the absence of conditions known to affect resting or hyperemic coronary blood flow. Increases in heart rate or preload reduced CFR because rCBFV was increased while hCBFV was unchanged. In contrast, changes in mean arterial pressure did not alter CFR. Proper interpretation of CFR measurements should take into account the hemodynamic conditions at which they are obtained. (Circulation 1990;81:1319-1330 The concept of coronary flow reserve, introduced 30 years ago by Coffman and Gregg,' provides a method for describing the capacity of the coronary circulation to conduct maximal hyperemic blood flow. The subsequent development

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Section: Previous Studiesmentioning

confidence: 99%

Interstudy variability of coronary flow reserve. Influence of heart rate, arterial pressure, and ventricular preload.

1990

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“…The findings of a detrimental influence of hypothyroidism on evolving infarction are not consistent with the expected findings ofa beneficial effect based on the hypothesis that hypometabolism caused by reduced thyroid availability would favorably alter the balance between myocardial oxygen consumption and demand by reducing metabolic rate (30). In part, this may be explainable, since metabolic rate appears to be a minor determinant of oxygen use compared to the energy requirements due to intramyocardial tension, contractile state, and heart rate (31,32). It is well established that thyroid hormone has direct and indirect intracellular actions that regulate the rate of metabolism (33,34).…”

Section: Discussionmentioning

confidence: 75%

Deleterious influence of hypothyroidism on evolving myocardial infarction in conscious dogs.

Karlsberg¹,

Friscia²,

Aronow³

et al. 1981

J. Clin. Invest.

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A B S T R A C T To study the influence of hypometabolism on evolving myocardial infarction in a model with intact autoregulation, we investigated 53 awake dogs after coronary artery occlusion. Severe hypothyroidism was induced by the intravenous administration of 1311. Animals were instrumented to obtain hemodynamic measurements, and regional myocardial blood flow was measured with radioactive microspheres. Infarct size was determined by the creatine kinase depletion method, and dysrhythmia analysis was performed from 24-h Holter monitor tapes in animals matched for infarct size. The microarchitecture of hypothyroid myocardium was determined by the electron microscope. Before coronary occlusion, mean systemic pressure in hypothyroid dogs was reduced by 14% and cardiac output reduced by 32%, with no change in left ventricular end-diastolic pressure, first derivative of left ventricular pressure rise, (dP/dt), or heart rate. After coronary occlusion, there was deterioration in hemodynamic measurements in both groups, with lower absolute levels of mean systemic blood pressure and cardiac output obtained in hypothyroid dogs. Hypothyroidism was detrimental to evolving infarction with a 36% increase in infarct size present in hypothyroid dogs (30±2%) compared to euthyroid controls (22±3%), P < 0.05. Dysrhythmias were more severe in hypothyroid dogs. There were no changes in the relationship between regional myocardial blood flow and the extent of infarction after coronary occlusion. Abnormalities in microarchitecture were present in hypothyroid dog myocardium. Severe hypometabolism in this model was associated with alterations in hemodynamics, more severe dysrhythmias and changes in microarchitecture. The combined effect of

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“…Previous studies in mature dogs have demonstrated that the major determinants of myocardial oxygen consumption in anesthetized mature dogs are contractility and wall stress, that external cardiac work and basal metabolism are quantitatively less important determinants, and that electrical activation accounts for less than 1 % of myocardial oxygen consumption (3,4,27,28,29). Parmley and Tyberg (30) has estimated that contractility and wall stress each account for 30-40% of total myocardial oxygen consumption in the basal state whereas external cardiac work and basal metabolism each may account for 10-20%.…”

Section: Discussionmentioning

confidence: 99%

β-Adrenergic Influence on Increased Myocardial Oxygen Consumption during Hypoxemia in Awake Newborn Lambs

Fisher

1989

Pediatr Res

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ABSTRACT. The purpose of this investigation was to Abbreviations determine the role of increased P-adrenergic activity in regulating the increase in myocardial oxygen consumption LVEDP, left ventricular and diastolic pressure that occurs during hypoxemia in unanesthetized newborn dP/dt, first derivative of left ventricular pressure lambs. Through a left thoracotomy, fluid-filled catheters LV, left ventricle were placed in the ascending aorta, coronary sinus and left atrium, a pressure transducer was introduced into the left ventricle, and pacing wires were sutured onto the left atrium. The lambs were studied 3 d later by making Acute hypoxemia has important effects on the developing intermittent m a~~r e m e n t s of aortic and coronary sinus myocardium. We have demonstrated previously that myocardial blood oxygen saturations and Hb concentrations, left ven-oxygen consumption increased by 30-40% during moderate tricular myocardial blood flow, cardiac output, heart rate, hypoxemia (Fio2 = 0.08-0.10) in unanesthetized newborn lambs left atrial and aortic blood Pressures, the nmximal first (1). To understand the underlying mechanism, we reasoned that derivative of left ventricular pressure, aortic and coronary hypoxemia also has been associated with P-adrenergically mesinus blood oxygen contents, the arteriovenous difference diated increases in several of the hemodynamic determinants of of oxygen across the left ventricular myocardium, myocar-myocardial oxygen consumption. Thus, we postulated that indial oxygen consumption, and external cardiac work (aortic creased 0-adrenergic activity would be an important regulator of mean blood Pressure times cardiac output). In nine lambs the increase in myocardial oxygen consumption that occurs with an intact P-adrenergic nervous system (group I), the during hypoxemia (2-7). above measurements were made during a control period Previous studies have demonstrated that myocardial oxygen and during hypoxemia (Fioz = 0.08-0.10) with sponta-consumption increased during hypoxemia in @-adrenergically neous tachycardia. In another group of 12 lambs (group blocked anesthetized newborn lambs and mature dogs (8, 9). 2), the measurements were made during a control period, However, all of these experimental animals were studied under after P-blockade (1.5 mg/kg intravenous propranolol) with the influence of @-blockade. Thus, there is no information using pacing at the control heart rate, during hypoxemia with the same experimental preparation with and without @-blockade pacing at the control heart rate, and during hypoxemia that would permit a quantitative estimation of the role of the Pwith pacing-induced tachycardia. In the group 2 lambs, P-adrenergically mediated augmentation of cardiovascular funcblockade completely inhibited the increase in heart rate, tion on the increase in myocardial oxygen consumption during maximal first derivative of left ventricular pressure, cardiac hypoxemia. Furthermore, the previous studies were performed output and cardiac work that ~~c~r r e d during hypo...

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

Cited by 261 publications

References 42 publications

Interstudy variability of coronary flow reserve. Influence of heart rate, arterial pressure, and ventricular preload.

Interstudy variability of coronary flow reserve. Influence of heart rate, arterial pressure, and ventricular preload.

Deleterious influence of hypothyroidism on evolving myocardial infarction in conscious dogs.

β-Adrenergic Influence on Increased Myocardial Oxygen Consumption during Hypoxemia in Awake Newborn Lambs

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