The Anrep Effect Reconsidered

Monroe, R. Grier; Gamble, W. J.; Lafarge, C. G.; Kumar, Avnish; Stark, James J.; Sanders, GL; Phornphutkul, Charlie; Davis, Micah

doi:10.1172/jci107074

Cited by 88 publications

(42 citation statements)

References 23 publications

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“…It might be expected that the Anrep effect also had a role in these early responses. 16 The Anrep effect has been related to the recovery from subendocardial ischemia by vascular autoregulation of the coronary bed, 17 and the extent of the Anrep effect in conscious dogs at slow heart rates was demonstrated to be less marked than at rapid heart rates, or after general anesthesia. 16 Studies of regional myocardial blood flow after sudden supravalvular aortic constriction have shown reversal of the epicardial to endocardial flow ratio associated with reduction in the diastolic pressure time per minute.…”

Section: Function Of Hypertrophied Heart /Sasayama Etalmentioning

confidence: 99%

Adaptations of the left ventricle to chronic pressure overload.

Sasayama¹,

Ross²,

Franklin³

et al. 1976

Circulation Research

260

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SUMMARY Left ventricular (LV) function during the adaptationto chronic pressure overload produced by an ascending aortic constriction was analyzed in conscious dogs, instrumented with intraventricular micromanometers and pairs of ultrasonic crystals for measurement of LV wall thickness (WTh) and internal LV chamber diameter. During inflation of the cuff to produce LV pressures averaging 220 mm Hg, calculated peak wall stress (WSt) increased by 55% above control while percent shortening decreased by 24% and mean circumferential shortening velocity (V CF ) decreased by 39% from control. By 9 days (mean) after aortic constriction, the cross-sectional area (CSA) of the LV wall increased by 10% and peak WSt fell to 37% above control. End-diastolic diameter (EDD) increased to 4% above control, while percent shortening and mean V CT remained reduced at -12% and -20% of control, respectively.During the phase of concentric hypertrophy (mean 2V-i weeks), CSA increased further to 15% above control and WSt fell to 22% above control, while EDD and percent shortening returned to control and mean V CF increased to -7 % of control (not significant). At 24 hours after release of the cuff WSt, percent shortening, mean V CP , and peak velocity of LV pressure rise (peak dP/dt) were not significantly different from control. Rapid, partial regression of hypertrophy was observed in some dogs. Thus, the left ventricle responds to chronically elevated pressure by initial dilation with increased WSt followed by gradual wall thickening and consequent reduction of WSt to near normal. After successful adaptation to the pressure overload, hypertrophy per se did not produce intrinsic depression of the myocardial inotropic state.THE PERFORMANCE of the heart and of cardiac muscle in chronic hypertrophy has been investigated intensively, but whether the myocardium of the intact hypertrophied left ventricle exhibits depression of the inotropic state has remained unresolved.1 In addition, little information is available concerning the time course of the functional adaptations that follow the application of a chronic pressure overload.The canine left ventricle is a useful model for the study of experimental circulatory lesions, but investigations of chronic pressure overloading produced by aortic constriction have been complicated by the frequent occurrence of aortic rupture. 2 We have overcome this problem in part by placing a Dacron graft beneath an inflatable aortic cuff; in addition, the ultrasonic technique for measurement of left ventricular (LV) regional dimensions 3 has been adapted to allow serial measurements of LV wall thickness (WTh) and internal diameter. This model for chronic pressure overload in the conscious dog has been applied to assess LV function before and during sustained inflation of the ascending aortic cuff over several weeks, and following its release. MethodsTwelve mongrel dogs weighing 19-36 kg (average, 26.7 kg) underwent right thoracotomy in the 4th intercostal space under sodium pentobarbital anesthesia (25 mg/kg, iv...

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Section: Function Of Hypertrophied Heart /Sasayama Etalmentioning

confidence: 99%

Adaptations of the left ventricle to chronic pressure overload.

Sasayama¹,

Ross²,

Franklin³

et al. 1976

Circulation Research

260

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“…According to present knowledge, other factors that may alter the dP/dt values after increasing AP are shortening deactivation (21)(22)(23)(24), the Anrep effect (15,18,19) and variations in coronary flow (25) or coronary perfusion pressure (26). Previous studies from our laboratory have shown that large increases of developed force (27) and coronary perfusion (28) do affect left ventricular performance in the intact canine left ventricle.…”

Section: Discussionmentioning

confidence: 88%

“…There is an initial impairment of contraction followed by improvement of ventricular performance until complete recovery. A reduction of the subendocardial coronary flow followed by restoration of myocardial perfusion seems to be implicated when the Anrep effect occurs in the intact heart (18,19). Complete cardiac influence of the Anrep effect is limited to a few minutes, and is certainly not present at the end of 10 min.…”

Section: Discussionmentioning

confidence: 99%

“…At present, two known factors are suggested as potentially affecting the rate of myocardial force generation when afterload changes: the Anrep effect (15,(18)(19)(20) and the shortening deactivation (21)(22)(23). Until (20) convincingly demonstrated the occurrence of the Anrep effect in muscle strips specially instrumented in order to obtain "physiological" contraction.…”

Section: Discussionmentioning

confidence: 99%

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The rate of force generation by the myocardium is not influenced by afterload

Fioretto¹,

Okoshi

et al. 1997

Braz J Med Biol Res

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The influence of afterload on the rate of force generation by the myocardium was investigated using two types of preparations: the in situ dog heart (dP/dt) and isolated papillary muscle of rats (dT/dt). Thirteen anesthetized, mechanically ventilated and thoracotomized dogs were submitted to pharmacological autonomic blockade (3.0 mg/ kg oxprenolol plus 0.5 mg/kg atropine). A reservoir connected to the left atrium permitted the control of left ventricular end-diastolic pressure (LVEDP). A mechanical constriction of the descending thoracic aorta allowed to increase the systolic pressure in two steps of 20 mmHg (conditions H 1 and H 2 ) above control values (condition C). After arterial pressure elevations (systolic pressure C: 119 ± 8.1; H 1 : 142 ± 7.9; H 2 : 166 ± 7.7 mmHg; P<0.01), there were no significant differences in heart rate (C: 125 ± 13.9; H 1 : 125 ± 13.5; H 2 : 123 ± 14.1 bpm; P>0.05) or LVEDP (C: 6.2 ± 2.48; H 1 : 6.3 ± 2.43; H 2 : 6.1 ± 2.51 mmHg; P>0.05). The values of dP/dt did not change after each elevation of arterial pressure (C: 3,068 ± 1,057; H 1 : 3,112 ± 996; H 2 : 3,086 ± 980 mmHg/s; P>0.05). In isolated rat papillary muscle, an afterload corresponding to 50% and 75% of the maximal developed tension did not alter the values of the maximum rate of tension development (100%: 78 ± 13; 75%: 80 ± 13; 50%: 79 ± 11 g mm -2 s -1 , P>0.05). The results show that the rise in afterload per se does not cause changes in dP/dt or dT/dt.

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“…The current concept about the Anrep effect is that, after a sudden increase in BP, a transient decrease of the inotropic capacity of the heart is observed, due to subendocardial ischemia. As a result of an autoregulatory vasodilation 15,32,33 , the perfusion of the heart is promptly restored, allowing the recovery of the inotropic capacity of the myocardium. As we performed the assessments of dP/dtmax a few seconds after the heart load (preload and afterload) underwent variation, there is a possibility that the Anrep effect might be responsible for the decrease in the values of dP/dtmax observed in some dogs in our study; that is, the evaluation of the dP/dt may have occurred during a period when a transient myocardial ischemia was taking place.…”

Section: Discussionmentioning

confidence: 99%

Influence of the elevation of the left ventricular diastolic pressure on the values of the first temporal derivative of the ventricular pressure (dP/dt)

Okoshi¹,

Fioretto²,

Bonatto³

et al. 1999

Arq. Bras. Cardiol.

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Purpose -To assess the effects of the elevation of the left ventricular end-diastolic pressure (LVEDP) on the value of the 1 st temporal derivative of the ventricular pressure (dP/dt). Methods (128±18.3mmHg and 150±21.5mmHg), diastolic blood pressure (98±16.9mmHg and 115±19.8mmHg), LVEDP (5.5±2.49 and 9.3±3.60mmHg), and dP/dt (4,855 ± 1,082 mmHg/s and 5,149±1,242mmHg/s) The rate of change in pressure with time (dP/dt), usually known as the 1 st temporal derivative of ventricular pressure, is one of the parameters employed for the assessment of the left ventricular function.In the 60's and 70's, the maximal values of dP/dt (dP/ dtmax) were largely employed to assess the inotropic capacity of the heart 1-4 . From the studies conducted at that time, it was suggested that dP/dt did not reliably reflect the inotropic state. The concept that finally prevailed was that dP/dtmax had limited practical applications as an indicator of the inotropic capacity 5 . The major limitation 6,7 was the lack of specificity of this parameter, since other factors, in addition to myocardial inotropic capacity, interfered with the maximal value of dP/dt. The factors capable of interfering with the values of the dP/dtmax include: the afterload 7,8 , the preload 9,10 and the presence of myocardial hypertrophy 2,11 . The correct interpretation of the relationship between the degree of myocardial stretching (preload) and dP/dt is particularly complex. According to the most traditional version of the concepts related to ventricular function, the inotropic capacity of the heart and the variation of the performance of the heart as a result of change in the muscular length during rest (Frank-Starling mechanism) were considered independent myocardial characteristics. Yet, the influence of the Frank-Starling mechanism on dP/dtmax would not be related to changes in the inotropic capacity of the heart. For this reason, variations in the ventricular volume occurring during the evaluation of dP/dt max would preclude an exact definition of the inotropic state.Advances in the knowledge of the physiological basis of myocardial contraction make this traditional view questionable, currently allowing alternative explanations. More recent information 12-17 about the subcellular adjustments involved in the relationship between the ventricular stretching during rest and the mechanical performance of the ventricles indicate that myocardial stretching interferes with the degree of activation of the contractile phenomenon, i.e., with myocardial contractility. The identification of

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The Anrep Effect Reconsidered

Cited by 88 publications

References 23 publications

Adaptations of the left ventricle to chronic pressure overload.

Adaptations of the left ventricle to chronic pressure overload.

The rate of force generation by the myocardium is not influenced by afterload

Influence of the elevation of the left ventricular diastolic pressure on the values of the first temporal derivative of the ventricular pressure (dP/dt)

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