Electrophysiological effects of transient aortic occlusion in intact canine heart

Benditt, D. G.; Kriett, Jolene M.; Tobler, H. Gareth; Gornick, Charles C.; Detloff, Barry L.S.; Anderson, Robert

doi:10.1152/ajpheart.1985.249.5.h1017

Cited by 18 publications

(11 citation statements)

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“…There is no consensus as to the effects of aortic constriction on action potential duration. Aortic constriction in the dog has been variously reported to shorten or to cause a minimal change in effective refractory period (Tobler, Gornick, Anderson & Benditt, 1986), and to prolong effective refractory period (Benditt et al 1985). In the pig, aortic constriction has been reported to shorten monophasic action potential duration (Jones & Lab, 1985;Dean & Lab, 1989b).…”

Section: Relation To Previous Investigationsmentioning

confidence: 99%

“…However, in all these studies the interventions employed were always unphysiological. These include distension of balloons in the cavity of the ventricle (Lerman, Burkhoff, Yue & Sagawa, 1985;Reiter, Synhorst & Mann, 1988), constriction of the aorta (Benditt, Kriett, Tobler, Gornick, Detloff & Anderson, 1985;Dean & Lab, 1989b) and direct stretching of the ventricular wall (Gornick, Tobler, Pritzker, Tuna, Almquist & Benditt, 1986;Gornick, Tobler, Tuna & Benditt, 1989). None of these approaches allows distinction to be made between possible effects of changes in preload and those of changes in afterload, and they do not provide quantitative information on contraction-excitation feedback in the physiologically ejecting heart.…”

Section: Introductionmentioning

confidence: 99%

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The effects of ventricular end‐diastolic and systolic pressures on action potential and duration in anaesthetized dogs.

Coulshed

Cowan

Drinkhill

et al. 1992

The Journal of Physiology

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SUMMARY1. Although it is known that mechanical events in the heart influence the duration of the cardiac action potential, there is no quantitative information on the effects of independent changes in ventricular end-diastolic and systolic pressures.2. Experiments were carried out on open-chest anaesthetized dogs in which the autonomic nervous influences on the heart were prevented and monophasic action potentials were recorded from the epicardial surface of the left ventricle. The duration of these action potentials was taken as the interval from the upstroke to the point of 90 % repolarization.3. Elevation of left ventricular peak systolic pressure, at constant end-diastolic pressure, significantly shortened the monophasic action potential.4. Elevation of end-diastolic pressure at constant peak systolic pressure significantly lengthened the monophasic action potential.5. Responses were not dependent on release of noradrenaline from sympathetic nerve terminals because they persisted after administration of bretylium tosylate. They were also not due to myocardial ischaemia because they persisted when coronary perfusion pressure was maintained at a constant high level.6. Simultaneous recordings of changes in myocardial segment length showed the expected responses to changes in ventricular pressures: increases in shortening in response to increases in diastolic pressure and no consistent effect from changes in systolic pressure.7. These investigations demonstrate the independent effects of changes in systolic and end-diastolic pressures on cardiac action potential duration. This effect is likely to be an effect of the mechanical events, i.e. contraction-excitation feedback. This response may be mediated through changes in myocardial fibre tension, the consequent changes in fibre shortening, or both.

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Section: Relation To Previous Investigationsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The effects of ventricular end‐diastolic and systolic pressures on action potential and duration in anaesthetized dogs.

Coulshed

Cowan

Drinkhill

et al. 1992

The Journal of Physiology

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“…8 (Lynch & Barry, 1989 (1963) and Lab (1982), and has since been expanded by many others (Boland & Troquet, 1980;Benditt, Kriet, Tobler, Gornick, Detloff & Anderson, 1985;Franz, Burkhoff, Yue & Sagawa, 1989;Hansen, Craig & Hondeghem, 1990;Calkins, Levine & Kass, 1991 ;Coulshed & Cowan, 1991). Mechanically activated ion channels have been implicated in the activation of cardiac ventricle (Hansen et al 1991; Le Guennec, White, Gannier, Argibay & Garnier, 1991), atrium (Kohl, Kamkin, Kiseleva & Streubel, 1992) and smooth muscle (Kirber, Walsh & Singer, 1988).…”

Section: Properties Of Macsmentioning

confidence: 99%

Stretch‐activation of rat cardiac myocytes

Craelius¹

1993

Experimental Physiology

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SUMMARYMechanically activated ion channels (MACs) in rat ventricular myocytes were activated by stretching membrane patches attached to microelectrodes. Charge injection from MACs, consisting mainly of inward K+, was sometimes of sufficient magnitude (0-2 pC) during brief (50 ms) periods, to trigger action currents. Action currents were shown to be extracellular records of action potentials. These results demonstrate the activation of myocytes by injection of approximately 4 pA from a few MACs in a membrane patch.

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“…'3 Seventeen preconditioned mongrel dogs (weight, [20][21][22][23][24][25] kg) were anesthetized with sodium pentobarbital (30 mg/kg i.v.) and mechanically ventilated with room air.…”

Section: Preparation Of Canine Infarctionmentioning

confidence: 99%

Effect of acute volume load on refractoriness and arrhythmia development in isolated, chronically infarcted canine hearts.

et al. 1989

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In normal isolated, perfused canine ventricles, increased ventricular volume leads to shortening of refractoriness. To test the hypothesis that myocardium within an infarction zone is more susceptible to volume-induced changes in refractoriness than is normal myocardium, we measured strength-interval curves at low and high end-diastolic volumes at control and infarcted sites in 14 isolated, blood perfused, canine hearts with chronic (> 25 days) infarctions. In addition, the effect of volume load on inducing ventricular arrhythmias was studied at one to six sites in 11 hearts. Differences in refractoriness and inducibility at low (22±5 ml) and high (48±6 ml) with elevated wall stress, increased volume load, and regional wall motion abnormalities.4,5 The mechanism of this association between these mechanical factors and arrhythmias has not been determined. Contraction-excitation feedback, the phenomenon whereby changes in the mechanics of myocardial contraction precede and result in changes in membrane potential, may contribute to arrhythmias. Alterations in the action potential duration, diastolic potential, conduction velocity, and automaticity have all been described under different loading conditions in myocardial tissue.6-11 These studies, however, were performed primarily in normal isolated tissues or under non-steady state conditions in intact normal hearts. The purpose of our study was to investigate this phenomenon in chronically infarcted canine ventricles, a model that may simulate the abnormal, scarred hearts in which malignant arrhythmias and congestive heart failure by guest on May 11, 2018 http://circ.ahajournals.org/ Downloaded from

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Electrophysiological effects of transient aortic occlusion in intact canine heart

Cited by 18 publications

References 0 publications

The effects of ventricular end‐diastolic and systolic pressures on action potential and duration in anaesthetized dogs.

The effects of ventricular end‐diastolic and systolic pressures on action potential and duration in anaesthetized dogs.

Stretch‐activation of rat cardiac myocytes

Effect of acute volume load on refractoriness and arrhythmia development in isolated, chronically infarcted canine hearts.

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