Analysis of systolic bulging. Mechanical characteristics of acutely ischemic myocardium in the conscious dog.

Amaki, Makoto; Weintraub, William S.; Schneider, R; Klein, Lloyd W.; Agarwal, Jai B.; Helfant, Richard H.

doi:10.1161/01.res.58.2.209

Cited by 88 publications

(26 citation statements)

References 31 publications

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“…14,32 However, in the present study, an increase in left ventricular enddiastolic volume resulted in further decreases in systolic area shrinkage and regional work in the ischemic region. This suggests that the ischemic region does not always behave as a completely passive material.…”

Section: Discussioncontrasting

confidence: 60%

Hyperkinesis without the Frank-Starling mechanism in a nonischemic region of acutely ischemic excised canine heart.

et al. 1988

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To determine the essential mechanism of increased systolic wall motion, i.e., hyperkinesis, in a nonischemic region (NIR) during acute ischemia, we simultaneously evaluated global and regional function ofthe excised, cross-circulated canine left ventricle connected to a volume servo pump before and after coronary occlusion. Regional areas were determined with pairs of orthogonal subendocardial sonomicrometers in the ischemic region (IR) and NIR. 468increased systolic segment shortening in a nonischemic region that correlated well with an increase in enddiastolic segment length and interpreted the increased shortening as a manifestation of a compensatory operation of the Frank-Starling mechanism. Thereafter, an increase in systolic segment shortening or wall thickening in a nonischemic region has been shown by many others5 8i and has been ascribed to either compensatory operation of the Frank-Starling mechanism or increased sympathetic activity. More recent studies by Lew et al.9 14 and Smalling et al. 15 have attributed the increased segment shortening to a combination of the Frank-Starling mechanism and mechanical unloading due to an intraventricular interaction between the ischemic and nonischemic regions. However, all these studies were performed in hearts in situ in which acute ischemia is usually accompanied by compensatory operation of the Frank-Starling mechanism and myocardial function is regulated by various neurohumoral mechanisms. This has made it difficult to separate the effects of the Frank-Starling mechanism and neurohumoral factors from other CIRCULATION by guest on

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Section: Discussioncontrasting

confidence: 60%

Hyperkinesis without the Frank-Starling mechanism in a nonischemic region of acutely ischemic excised canine heart.

et al. 1988

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“…All length values were normalised by assuming segment length at end diastole in control to be 10 mm. 18 …”

Section: Sonomicrometrymentioning

confidence: 99%

Acute pulmonary microembolism induces different regional changes in preload and contraction pattern in canine right ventricle

Zwißler¹,

Forst²,

Meßmer³

1990

Cardiovascular Research

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Correspondence Letters containing critical assessments of material published in Cardiovascular Research, including reviews, will be considered for publication. They should be sent to the Editor within 6 months of the appearance of the article concerned.Rapid publication Short papers will be considered for rapid publication (within 3 months). These should contain material which merits accelerated publication and must not occupy more than 4 journal pages, including tables, figures and references (authors are responsible for assessing the length accurately before submission). Current standard section headings should be used. Abstracts should not exceed 100 words, and there should not be more than 10 references. Papers submitted for rapid publication should be clearly marked as such. Rejection does not preclude resubmission as a full paper. No proofs will be sent, so the submitted copy must be entirely correct.Instructions to authors. These are printed in full annually in the January issue. The following should act as a guide, but authors are urged to consult the full instructions as papers that do not comply will be returned for revision.SI Units All units of measurement, except for blood pressures, should be in SI (including those in the figures). Blood pressures should be expressed in mm Hg.References should be typed (double spacing) on separate sheets. Contributors are responsible for the accuracy of their references.

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“…In the work of Akaishi et al 4 and that of Lew et al ,8 the influence of preload on the movement of ischemic and nonischemic myocardium was demonstrated. In the present study we undertook the analysis of the influence of afterload on systolic bulging and augmentation of nonischemic myocardium.…”

mentioning

confidence: 95%

“…1 4 showed how bulging occurred predominantly during isovolumetric shortening and that the slight inward motion of ischemic myocardium during ejection systole was passive. They further demonstrated that the extent of bulging depended on preload, and this dependence could be explained by the exponential shape of the tension-length relationship.…”

mentioning

confidence: 99%

The effect of changes in afterload on systolic bulging.

et al. 1988

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It has been previously shown that after acute coronary occlusion, the extent of systolic bulging is dependent on preload and the function of the remote nonischemic myocardium is influenced by the motion of the ischemic myocardium as well as by the loading conditions. To examine the isolated effects of changing afterload on the movement of acutely ischemic and nonischemic myocardium, seven open-chest, anesthetized dogs were paced from the left atrium at a rate of 100 beats/min after crushing of the sinus node. The pulmonary artery was perfused artificially and the left ventricular end-diastolic pressure (LVEDP) was carefully controlled with a right heart bypass system. Twenty minutes after occlusion of the left anterior descending artery, the peak left ventricular pressure (LVP) was adjusted to three levels (70, 90, and 110 mm Hg) by blood withdrawal or aortic constriction, while the LVEDP was kept constant (8.3 + 2.3 mm Hg). Segment length in the ischemic (IZ) and nonischemic zones (NZ) were measured with sonomicrometers and total, isovolumetric, and ejection systolic shortening (%zXL) were calculated. Changes in left ventricular minor-axis diameter were measured with diameter crystals. Increasing the peak LVP increased the LVP both at aortic valve opening and closing. To keep the LVEDP constant as peak LVP was increased, the cardiac output had to be decreased (p < .0001).In the IZ, increasing the peak LVP increased isovolumetric bulge (-13.6 + 3.4%, -14.4 ± 3.7%, and -15.0 3.7% at LVP 70, 90, and 110 mm Hg, respectively, p < .00005) and decreased ejection %AL (4.8 4.6%, 4.1 ± 4.3%, and 3.3 ± 4.4%, p < .05) so that total %AL was decreased (p < .001). In the NZ, increasing the peak LVP decreased both isovolumetric %AL (8.4 ± 2.7%, 7.1 + 2.9% and 6.3 ± 2.8%, p < .0005) and ejection %zSL (10.8 ± 6.5%, 9.6 + 4.4%, and 8.8 ± 4.2%, p < .05) so total %AL was reduced (p < .0005). We conclude that increasing afterload increases the extent of the bulge in the ischemic zone and hypothesize that these changes are caused directly by an increase in wall tension. Increasing afterload also decreases shortening in nonischemic myocardium. Circulation 77, No. 1, 221-226, 1988

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Analysis of systolic bulging. Mechanical characteristics of acutely ischemic myocardium in the conscious dog.

Cited by 88 publications

References 31 publications

Hyperkinesis without the Frank-Starling mechanism in a nonischemic region of acutely ischemic excised canine heart.

Hyperkinesis without the Frank-Starling mechanism in a nonischemic region of acutely ischemic excised canine heart.

Acute pulmonary microembolism induces different regional changes in preload and contraction pattern in canine right ventricle

The effect of changes in afterload on systolic bulging.

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