Left ventricular pressure and norepinephrine efflux from the innervated heart

Lafarge, C. G.; Monroe, RG; Gamble, W. J.; Rosenthal, Amnon; Hammond, RP

doi:10.1152/ajplegacy.1970.219.2.519

Cited by 17 publications

(5 citation statements)

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“…However, the lack of change in heart rate in our study suggested that there was probably little or no increase in catecholamine release into the systemic circulation and failed to support activation of sympathetic nervous system after PAB as an important mechanism for the improved RV contractility. However, in our study one cannot rule out the possibility of catecholamine release from the myocardium per se after acute afterload increase, which was clearly demonstrated to be the case by experiments in the intact heart (LaFarge et al 1970). However, in our study one cannot rule out the possibility of catecholamine release from the myocardium per se after acute afterload increase, which was clearly demonstrated to be the case by experiments in the intact heart (LaFarge et al 1970).…”

Section: Neurohumoral Factorscontrasting

confidence: 69%

“…Additionally, the sympathetic nervous system was shown not to in¯uence the increase in the slope of the ESPVR of the canine LV to increasing afterload in an experiment involving bilateral ablation of the stellate ganglia (Schipper et al 1993). However, in our study one cannot rule out the possibility of catecholamine release from the myocardium per se after acute afterload increase, which was clearly demonstrated to be the case by experiments in the intact heart (LaFarge et al 1970).…”

Section: Neurohumoral Factorscontrasting

confidence: 51%

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Acute effects of pulmonary artery banding in sheep on right ventricle pressure–volume relations: relevance to the arterial switch operation

Hon

Steendijk

Khan

et al. 2001

Acta Physiologica Scandinavica

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The first stage of the two-stage arterial switch operation (ASO) for transposition of the great arteries (TGA) is associated with depressed ventricular function and an unstable immediate post-operative course. It is unclear if this is because of the acute increase in afterload of the thin-walled, low-pressure ventricle by pulmonary artery banding (PAB). To determine the acute effects of afterload increase on the contractile function of thin-walled ventricles, we studied the right ventricular pressure-volume relations of seven sheep before and 30 min after PAB using combined pressure-conductance catheters during inflow reduction. Load independent indices of systolic and diastolic performance were derived from these relations. Pulmonary artery banding increased the mean ratio between right and left ventricular systolic pressure from 0.34 +/- 0.05 to 0.64 +/- 0.10, P < 0.05 (mean +/- SD). There were no significant changes in heart rate and end-systolic volume after banding although there was an incremental trend in the end-diastolic volume and stroke volume. Right ventricular output (530 +/- 163-713 +/- 295 mL min (-1), P < 0.05), slope of the end-systolic pressure-volume relation (ESPVR) (3.7 +/- 2.8-10.0 +/- 4.8 mmHg mL (-1), P < 0.05) and slope of the pre-load recruitable stroke work (PRSW) relation (9.6 +/- 1.8-15.0 +/- 3.1 mmHg, P < 0.05) were significantly increased indicating improved contractile state after banding. The diastolic function curve was unchanged after banding although the right ventricle (RV) was operating at a larger end-diastolic volume. Hence, the RV of sheep responded to acute pressure overload by demonstrating enhanced contractility and evidence of the Frank-Starling mechanism without associated change in right ventricular diastolic performance.

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Section: Neurohumoral Factorscontrasting

confidence: 69%

Section: Neurohumoral Factorscontrasting

confidence: 51%

Acute effects of pulmonary artery banding in sheep on right ventricle pressure–volume relations: relevance to the arterial switch operation

Hon

Steendijk

Khan

et al. 2001

Acta Physiologica Scandinavica

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“…A further possibility, suggested from previous studies in isolated dog hearts, is that shortening of action potential following increases in LVPP may have been secondary to release of noradrenaline from endogenous stores at sympathetic nerve endings (Monroe, LaFarge, Gamble, Hammond & Morgan, 1966). This effect has also been demonstrated in vivo (LaFarge, Monroe, Rosenthal & Hammond, 1970). However we showed that, even following administration of bretylium tosylate which blocks the release of noradrenaline from sympathetic nerve endings (Gilman, Goodman, Rall & Murad, 1985) changes in action potential duration still occurred in response to changes in either LVEDP or LVPP.…”

Section: Discussionmentioning

confidence: 94%

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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“…Conversely, β receptor antagonism curtails mechanically induced arrhythmia 28 . Moreover, raised intraventricular pressure releases catecholamines from the ventricle 29 and this could promote mechanically induced arrhythmia.…”

Section: At the Channel Levelmentioning

confidence: 99%

Mechanosensitive‐Mediated Interaction, Integration, and Cardiac Control

Lab

2006

Annals of the New York Academy of Sciences

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This review covers aspects of the cardiac mechanotransduction field at different levels, and advocates the possibility that mechanoelectro-chemical transduction forms part of a network of mechanically linked integration in heart-mechanically mediated integration (MMI). It assembles evidence and observations in the literature to promote this hypothesis. Mechanical components can provide the bond between interactions at molecular, cellular, and macro levels to enable the integration. Stretch-activated channels (SACs) exist in the heart, but stresses and strains can affect other membrane channels or receptors. A cellular mechanical change can thus promote several ionic or downstream changes. Cell signal cascades have been implicated and can affect membrane electrophysiology. MMI could shape intracellular and downstream signals using the cytoskeleton and intracellular Ca(2+). MMI also spans other regulatory systems and processes such as the autonomic nervous system (ANS) and operates throughout the whole heart as an integrative system. Finally, supporting the hypothesis, if elements of the normal integration become deranged it contributes to cardiovascular disease and, potentially, lethal arrhythmia.

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Left ventricular pressure and norepinephrine efflux from the innervated heart

Cited by 17 publications

References 0 publications

Acute effects of pulmonary artery banding in sheep on right ventricle pressure–volume relations: relevance to the arterial switch operation

Acute effects of pulmonary artery banding in sheep on right ventricle pressure–volume relations: relevance to the arterial switch operation

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

Mechanosensitive‐Mediated Interaction, Integration, and Cardiac Control

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