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Control of stroke volume and cardiac output
Published in Neil Herring, David J. Paterson, Levick's Introduction to Cardiovascular Physiology, 2018
Neil Herring, David J. Paterson
The reader may have come away from Chapters 3 and 4 with the impression that a stronger heartbeat must always be due to a rise in cytoplasmic Ca2+; but this is not so. Figure 6.4 shows the effect of diastolic stretch on twitch force and the cytoplasmic Ca2+ transient. Stretch causes an immediate force increase, with no increase in the systolic Ca2+ tran-sient, unlike the Ca2+-mediated effect of catecholamines (Sections 3.8 and 4.5). If the stretch is maintained, there is a further slow increase in force over ~5 min, which is due to increased Ca2+ transients. The immediate force increase accounts for 60% of the eventual response and is the basis of the length–tension relation. The subsequent Ca2+-mediated slow force response underlies the Anrep effect in intact hearts (Section 6.9).
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.