Measurement of myocardial developed tension and its relation to oxygen consumption

Rh, McDonald; Taylor, RR; Cingolani, H.E.

doi:10.1152/ajplegacy.1966.211.3.667

Cited by 95 publications

(30 citation statements)

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“…Shortly thereafter, Evans and Matsuoka (2) concluded from studies on the dog heart-lung preparation.that "there is a relation between the tension set up on contraction and the metabolism of the contractile tissue." These demonstrations, that tension 2 development is an important determinant of MVo2, have been verified repeatedly (3)(4)(5)(6)(7)(8). It has also been proposed that the heart's oxygen utilization is determined primarily by a closely related variable, the work performed by the contractile elements (CEW) (9).…”

Section: Introductionmentioning

confidence: 78%

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: Introductionmentioning

confidence: 78%

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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“…The presence of fully developed transmural gradients in lactate and creatine phosphate when flow was stopped for only 15 seconds and the significant changes found in all metabolites, including ATP, when flow was stopped for 30 seconds indicate that the metabolic changes in the myocardium were intimately related to the energy needs of the ventricle as regulated by the existing loading conditions. The significantly elevated ventricular end-diastolic and systolic pressures produced by volume loading undoubtedly resulted in a substantially increased wall stress, which is a primary determinant of the myocardial energy needs (31). The elevated enddiastolic pressure might be of particular significance if increasing ventricular filling pressure preferentially moves the inner region sarcomeres closer to the peak of their active length-tension curve, as suggested by Yoran et al (32).…”

Section: Discussionmentioning

confidence: 96%

Transmural gradients in ventricular tissue metabolites produced by stopping coronary blood flow in the dog.

Dunn¹,

Griggs²

1975

Circulation Research

120

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To determine whether transmural metabolite gradients develop in the contracting, ischemic left ventricle due to factors other than a nonuniform distribution of myocardial blood flow, right and left coronary artery inflow was completely stopped with vessel occluders in open-chest dogs for 15 or 30 seconds before a transmural myocardial tissue sample was obtained for regional analysis of creatine phosphate, adenosine triphosphate (ATP), and lactate. Heart rate was controlled, and the decline in left ventricular systolic pressure during the period in which coronary blood flow was stopped was attenuated by aortic constriction. Studies were also performed in dogs that were (1) pretreated with propranolol, (2) subjected to ventricular fibrillation, and (3) volume loaded. Control studies revealed no transmural metabolite gradients in the normally perfused ventricle, but creatine phosphate was slightly lower in the inner region than it was in the outer and middle ventricular wall regions. With coronary blood flow stopped for 30 seconds, a significant lactate gradient, increasing from the outer to the inner region, was present. Propranolol-treated dogs with their coronary blood flow stopped for 30 seconds also exhibited a lactate gradient, but dogs with ventricular fibrillation and their coronary blood flow stopped for 30 seconds did not. Volume-loaded dogs with their coronary blood flow stopped for only 15 seconds had a significant lactate gradient. Reciprocal gradients occurred in creatine phosphate but not in ATP. The findings suggest that the contracting ventricle uses energy unevenly and that in myocardial ischemia one of the factors causing greater subendocardial vulnerability is a greater energy need in this region.• Previous studies from this laboratory have shown that metabolic changes occurring in the left ventricle because of inadequate coronary blood flow are greater in the subendocardium than they are in the subepicardium (1-4). This difference has been attributed primarily to nonuniform systolic compression of the coronary vessels (5, 6) which results in a greater impairment of subendocardial blood flow than it does of subepicardial blood flow (7,8). However, the possibility also exists that other factors, such as a higher subendocardial energy requirement (9-12), a greater capacity of subendocardial tissue cells for glycolysis (13,14), or greater subendocardial beta-adrenergic stimulation, contribute to the uneven metabolic response. The primary purpose of the present study was to investigate these possibilities in open-chest dogs by examining regional metabolite levels in the left ventricle after blood flow had been completely stopped in both the left and right coronary arteries for a brief but metabolically significant interval of time. Heart rate was controlled, and the decline in This work was supported by U. S. Public Health Service Grant HL 11876 from the National Heart and Lung Institute and by the Missouri Heart Association.Received April 7, 1975. Accepted for publication June 30, 1975. ...

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“…The increased 2DG uptake into the heart muscle may also be interpreted in relation to oxygen consumption in this muscle. Previous studies reported that there existed high correlations between oxygen consumption and some parameters related to tension in the heart muscle (BRITMAN and LEVINE, 1964;MCDONALD et al, 1966;SARNOFF et al, 1958 ;SUGA et al, 1980;WEBER and JANICKI, 1977). Therefore, the large amount of 2DG uptake into the left ventricular wall may be considered to be correlated with a high tension developed in this muscle.…”

mentioning

confidence: 89%

Radioactive deoxyglucose uptake into the heart muscle of the monkey.

Matsunami

1982

Jpn.J.Physiol

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Measurement of myocardial developed tension and its relation to oxygen consumption

Cited by 95 publications

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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

Transmural gradients in ventricular tissue metabolites produced by stopping coronary blood flow in the dog.

Radioactive deoxyglucose uptake into the heart muscle of the monkey.

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