Letter to the editor: The venous circulation actively alters flow: a brief evolutionary perspective

Letter to the EditorIntegrative Cardiovascular Physiology and PathophysiologyLetter to the editor: The venous circulation actively alters flow: a brief evolutionary perspectiveJon-Emile S. KennyJon-Emile S. KennyHealth Sciences North Research Institute, Sudbury, Ontario, CanadaFlosonics Medical, Sudbury, Ontario, CanadaPublished Online:15 Jan 2021https://doi.org/10.1152/ajpheart.00862.2020MoreSectionsPDF (152 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations In a recent issue of the American Journal of Physiology-Heart and Circulatory Physiology, Dr. Brengelmann uses an elegant mathematical model of the circulation to criticize certain tenets of the widely taught Guytonian approach (1). In Dr. Brengelmann’s model, blood flow is an independent variable for which the heart is the sole energy source. The arterial and venous vascular beds have resistances, compliances, and capacitances, which are also independent variables. Consequently, the volumes and pressures that evolve within vascular compartments are dependent variables.With this ontology, he illustrates mathematically that increasing arterial resistance (without changing vascular capacitance) retains blood volume in arteries relative to veins, which diminishes right atrial pressure for any given flow. Conversely, reducing resistance (while simultaneously increasing arterial and venous capacitance) distributes volume preferentially into venous “resting volume” such that right atrial pressure also falls for any given flow.Yet, Dr. Brengelmann does not entertain the venous vasculature adding energy to the system. This appears acceptable because, as above, the ontological assumptions of his model place the heart as the sole energy source and the vasculature as a series of malleable conduits through which energy is stored and dissipated, but not generated; this is an oversimplification.More than half of a billion years ago, genes encoding contractile elements (e.g., actin, myosin, troponin) emerged (2). Importantly, these proteins predate the Earth’s first heartbeat by tens of millions of years. The first closed circulations—modeled by today’s Amphixious—lacked a heart; blood moved by contractile vascular segments powered by myoepithelial cells (3). Approximately 450 million years ago, the first primitive hearts appeared, as exemplified by contemporary hagfish (2). Like all primitive fish, there is no pumping chamber on the arterial side of the circulation—it is all venous. Hagfish have three accessory venous hearts that boost venous effluent to the branchial (i.e., systemic) heart—which then moves blood to the gills for oxygenation. The posterior cardinal vein (analogous to the portal vein) itself contracts and aids filling of the accessory, portal venous heart, which then jettisons venous blood across the liver. Neither the branchial nor the portal venous hearts have coronary circulations and they are mediated locally by granules filled with catecholamines (4, 5). Hagfish placed into hypertonic saline lose blood volume and their hemodynamic response is to release local norepinephrine and decrease venous capacitance (5). This maintains central venous tone and “vis‐a‐tergo” filling (force from behind) of their portal venous and branchial hearts (4).The evolutionary provenance of moving blood lies in the venous vasculature. From these beginnings, amphibian, avian, and mammalian systems evolved cardiovascular complexity (6). I appreciate Dr. Brengelmann’s theses that all clinical hemodynamic models belie authenticity, that (in the steady state) blood flow may be mathematically described by the pressure gradient between other vascular segments and that the terms “stressed” and “unstressed” volumes are sloppy. But to overlook the venous vasculature’s specific role as an independent mover of blood in the mammalian circulatory system is to ignore basic clinical hemodynamics (7, 8) and our evolutionary history.DISCLOSURESDr. Kenny is the Co-founder and Chief Medical Officer of Flosonics Medical.AUTHOR CONTRIBUTIONSJ-E.S.K. drafted manuscript; edited and revised manuscript; and approved final version of manuscript.REFERENCES1. Brengelmann GL. Venous return and the physical connection between distribution of segmental pressures and volumes. Am J Physiol Heart Circ Physiol 317: H939–H953, 2019. doi:10.1152/ajpheart.00381.2019. Link | ISI | Google Scholar2. Stephenson A, Adams JW, Vaccarezza M. The vertebrate heart: an evolutionary perspective. J Anat 231: 787–797, 2017. doi:10.1111/joa.12687. Crossref | PubMed | ISI | Google Scholar3. Moller PC, Philpott CW. The circulatory system of amphioxus (Branchiostoma floridae) I. Morphology of the major vessels of the pharyngeal area. J Morphol 139: 389–406, 1973. doi:10.1002/jmor.1051390403. Crossref | PubMed | ISI | Google Scholar4. Farrell AP. Cardiovascular systems in primitive fishes. Fish physiology 26: 53–120, 2007. doi:10.1016/S1546-5098(07)26002-9.Crossref | Google Scholar5. Foster JM, Forster ME. Changes in plasma catecholamine concentration during salinity manipulation and anaesthesia in the hagfish Eptatretus cirrhatus. J Comp Physiol B 177: 41–47, 2006. doi:10.1007/s00360-006-0107-6. Crossref | PubMed | ISI | Google Scholar6. Furst B. The heart: pressure-propulsion pump or organ of impedance? J of Cardiothorac and Vasc Anesth 29: 1688–1701, 2015. doi:10.1053/j.jvca.2015.02.022. Crossref | PubMed | ISI | Google Scholar7. Rothe CF. Mean circulatory filling pressure: its meaning and measurement. J Appl Physiol 74: 499–509, 1993. doi:10.1152/jappl.1993.74.2.499. Link | ISI | Google Scholar8. Tyberg JV. How changes in venous capacitance modulate cardiac output. Pflugers Archiv 445: 10–17, 2002. doi:10.1007/s00424-002-0922-x. Crossref | PubMed | ISI | Google ScholarAUTHOR NOTESCorrespondence: J-E. S. Kenny ([email protected]org). Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation CollectionsAJP-Heart CollectionsIntegrative Cardiovascular Physiology and PathophysiologyThis collection contains research and reviews of cardiovascular function at all levels of organization, ranging from the intact and integrative animal and organ function to the cellular, subcellular, and molecular levels. Cited ByHow to end the ‘venous return’ controversyEuropean Journal of Anaesthesiology, Vol. 39, No. 7 More from this issue > Volume 320Issue 1January 2021Pages H469-H470 Crossmark Copyright & PermissionsCopyright © 2021 the American Physiological Societyhttps://doi.org/10.1152/ajpheart.00862.2020PubMed33448258History Received 26 October 2020 Accepted 27 October 2020 Published online 15 January 2021 Published in print 1 January 2021 Keywordsblood flowevolutionaryhemodynamicsprimitive fishvenous return Metrics

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