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Orthotopic Cardiac Transplantation
Published in David Robertson, Italo Biaggioni, Disorders of the Autonomic Nervous System, 2019
Aside from stimulation of β-receptors by circulating catecholamines, mechanisms of increased ventricular contractility in the transplant patient are, of necessity, non-neural. The intrinsic Frank-Starling effect, already mentioned, effectively increases heart output as the input increases. The Bowditch treppe effect is another non-neural mechanism in which (by poorly known mechanisms) an increase in heart rate, from whatever cause, produces an increase in contractile force. The Bowditch effect was more apparent in intact anaesthetized dogs than in conscious control dogs (Higgins et al., 1973), and has probably been demonstrated to be clinically significant in transplant patients (Ricci et al., 1979). Moreover, as noted by Traill (1990), the Bowditch effect may be a source of experimental error in studies of ventricular function when rate is not controlled. Another factor to be considered (Kent and Cooper, 1974) is the Anrep effect. This is the intrinsic property of the heart to increase its contractile force as the aortic pressure (afterload) increases, independent of ventricular end diastolic volume. However the Anrep effect was not observed in transplant patients performing isometric exercise (see below). A clear elevation arterial pressure with no change in heart rate was not associated with a change in left ventricular contractility or cardiac output as measured by Doppler echocardiography (Robson et al., 1989).
The cardiac myocyte: excitation and contraction
Published in Neil Herring, David J. Paterson, Levick's Introduction to Cardiovascular Physiology, 2018
Neil Herring, David J. Paterson
The amount of Ca2+ in the SR store depends on the balance between the influx of extracellular Ca2+ during the plateau and its expulsion during diastole. Consequently, Ca2+ store size depends on:extracellular Ca2+ concentration, which is normally very stable;the size of the L-type Ca2+ current, which is increased by the β1-adrenoceptor ligands, noradrenaline and adrenaline, and reduced by Ca2+ channel blockers;heart rate, which affects the duration of systole (extracellular Ca2+ influx) relative to diastole (Ca2+ expulsion). Store size and contractile force generally increase with heart rate, as described under ‘Bowditch effect’ (see Section 6.11).
Emerging therapeutic targets for cardiac hypertrophy
Published in Expert Opinion on Therapeutic Targets, 2022
Alexander J. Winkle, Drew M. Nassal, Rebecca Shaheen, Evelyn Thomas, Shivangi Mohta, Daniel Gratz, Seth H. Weinberg, Thomas J. Hund
The heart has evolved a robust system for responding to acute and chronic changes in demand. Assuming that efficiency of blood as an O2 carrier is a constant (not true in all cases, elite athletes, for example), the heart can meet increased demand by either increasing heart rate or stroke volume [cardiac output is the product of heart rate and stroke volume]. The prevailing paradigm is that the heart is sensitive to changes in both preload (an external mechanical stress applied in the axial direction of the muscle fibers), and afterload (the mechanical impedance of the vasculature). Acute, physiological changes in load are negotiated in part through passive reflexes that increase stroke volume without requiring changes in cardiac structure – the Frank-Starling mechanism describes a length–tension relationship observed in striated muscle that impacts intrastroke contractility. Application of a preload to a muscle fiber can vary the tension generated by that fiber. For each fiber there exists an optimal length that maximizes the inotropic state [12], the result of this being an organ that can produce a response compensatory to its volumetric state. The underlying mechanisms are not yet fully understood but are believed to be related to stretch-activated regulation of calcium [13]. The Anrep effect is a similar compensatory mechanism that is observed following an increase in afterload. When mechanical impedance of the vasculature is increased, on the timescale of 10–15 minutes an increase in calcium transient amplitude is observed, also described as the slow force response [14]. A third intrinsic inotropy-regulating mechanism exists, known as the Bowditch effect. Where the Frank-Starling and Anrep effects are regulated through mechanical strain, the Bowditch effect is instead dependent on heart rate, and describes an increase in force generation as a function of increased rate.