Physical factors and cardiac adaptation

Jp, Gilmore; He, Chao; Rr, Taylor; Rh, McDonald

doi:10.1152/ajplegacy.1966.211.5.1219

Cited by 29 publications

(16 citation statements)

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“…First, the Anrep effect is not seen in papillary muscle preparations (8,11 (23,24), making it necessary for the ventricle to rely heavily on the compensatory mechanism of vascular autoregulation to avoid ischemia, a mechanism that requires time.…”

Section: Resultsmentioning

confidence: 99%

“…Despite the fact that Sarnoff et al showed an efflux of potassium from the heart after a sudden increase in systolic pressure (10) Blinks and Koch-Weser pointed out differences between the Anrep effect and the Bowditch effect, making it doubtful that similar mechanisms were involved. Foremost in these differences was the observation that the Anrep effect is not found in cardiac muscle strip preparations (8,11).…”

mentioning

confidence: 99%

“…Mindful of the findings of Blinks and Koch-Weser (8) as well as Gilmore, Cingolani, Taylor, and McDonald (11) that the effect is not seen in muscle strip preparations, but only seen in intact hearts, and mindful that coronary flow is not present in muscle strip preparations it was decided to attempt to study, in depth, the interrelationships of coronary flow and the "Anrep" effect using an isolated heart preparation. From these studies evidence was obtained which suggests that the "Anrep" effect, rather than being due to an increased state of contractility or intrinsic adaptation that appears subsequent to an abrupt increase in ventricular pressure (5)(6)(7)(8)(9)(10)(11)14), is more accurately described as the recovery from a negative inotropic effect caused by the abrupt increase.…”

mentioning

confidence: 99%

“…From these studies evidence was obtained which suggests that the "Anrep" effect, rather than being due to an increased state of contractility or intrinsic adaptation that appears subsequent to an abrupt increase in ventricular pressure (5)(6)(7)(8)(9)(10)(11)14), is more accurately described as the recovery from a negative inotropic effect caused by the abrupt increase. Further evidence was obtained suggesting that subendocardial ischemia is responsible for the negative inotropic effect, a condition which is stubsequently corrected by vascular autoregulation of the coronary bed with a redistribution of coronary flowr.…”

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confidence: 99%

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The Anrep Effect Reconsidered

Monroe¹,

Gamble²,

Lafarge³

et al. 1972

J. Clin. Invest.

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

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confidence: 99%

mentioning

confidence: 99%

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The Anrep Effect Reconsidered

Monroe¹,

Gamble²,

Lafarge³

et al. 1972

J. Clin. Invest.

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“…It is well known that large changes in tension development can alter diastolic stiffness through a mechanism involving stress relaxation (1)(2)(3)(4)(5). Effects (6)(7)(8)(9)(10)(11).…”

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confidence: 99%

Influence of acute myocardial depression on left ventricular stiffness and its elastic and viscous components.

Templeton¹,

Wildenthal²,

Willerson³

et al. 1975

J. Clin. Invest.

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A B S T R A C T The influence of acute myocardial depression on ventricular stiffness and on its elastic and viscous components was studied in 19 dogs. After the animals were placed on cardiopulmonary bypass, stiffness was measured by sinusoidally injecting volume changes of 0.5 ml (AV) at 22 Hz into paced, isovolumically contracting left ventricles and determining the amplitude (AP) of the sinusoidal pressure response. Stiffness was linearly related to pressure (P) throughout the cardiac cycle, so that AP/AV = aP + A, where a and i are constants. Myocardial depression was induced in one of three different ways: by coronary artery ligation, by administration of propranolol (Inderal), or by administration of pentobarbital. All three interventions caused significant increases in the slope, a, of the stiffness-pressure relationship, while the intercept, A, remained unchanged. Release of the coronary occlusion or administration of acetylstrophanthidin partially reversed depression and the change in a. Approximation of the mechanical nature of the left ventricle in terms of a linear second-order mechanical system permitted the division of stiffness into its elastic and viscous components. Like total stiffness, both the elastic and the viscous components were linearly related to ventricular pressure. Elastic stiffness was not changed, but the slope of the line relating viscous stiffness to pressure was significantly increased during ischemic depression, Dr. Wildenthal holds a Research Career Development Award (HL 70125)

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