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• W2016985946 abstract "POINT-COUNTERPOINT COMMENTSThe following letters are in response to the Point:Counterpoint series “Hypoxic pulmonary vasoconstriction is/is not mediated by increased production of reactive oxygen species” that appears in this issue.Wayne MitznerWayne MitznerPublished Online:01 Oct 2006https://doi.org/10.1152/japplphysiol.00794.2006This article has been correctedMoreSectionsPDF (41 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat To the Editor: The underlying issue being discussed (1a, 4) seems much broader than simply the role of venoconstriction. It is really about the regulation of the magnitude of cardiac output. Thus while the argument put forth by Hainsworth and Drinkhill is fine as far as it goes, it fails to address how it is that cardiac output can rise to four or five times its baseline level. If, as they claim, the blood volume in the splanchnic bed is flow dependent, then how can the cardiac output increase so much? Similarly, although Rothe cites evidence for volume shifts resulting from active vascular constriction, the maximal magnitude of these shifts is not nearly sufficient to account for such extreme increases in cardiac output.Because it is axiomatic that the heart cannot pump any faster than the periphery can return blood to it, this then leaves us with the question as to how does the Pmcf increase during exercise? One possibility noted many years ago is that the heart itself can translocate sufficient volume to the periphery to substantially increase cardiac output (3). Another mechanism does not actually involve the Pmcf at all, but rather, the effective resistance to venous return. As theoretically and experimentally documented by Caldini et al. and others (1, 2), simply opening a relatively noncompliant A-V shunt (such as in a stiff contracting muscle) will significantly decrease this resistance, thereby increasing venous return and cardiac output. It is for these reasons that one needs neither much active venoconstriction nor any significant splenic contraction, to achieve substantial increases in cardiac output. Thus it seems that both sides of this pro/con debate are correct and that there really isn't much controversy at all.REFERENCES1 Caldini P, Permutt S, Waddell JA, and Riley RL. Effect of epinephrine on pressure, flow, and volume relationships in the systemic circulation of dogs. Circ Res 34: 606–623, 1974.Crossref | PubMed | ISI | Google Scholar1a Hainsworth R and Drinkhill M. Counterpoint: Active venoconstriction is not important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis. J Appl Physiol. In press.Google Scholar2 Mitzner W and Goldberg H. The effect of epinephrine on the resistive and compliant properties of the canine systemic vasculature. J Appl Physiol 39: 272–280, 1975.Link | ISI | Google Scholar3 Mitzner W, Goldberg H, and Lichtenstein S. Effect of thoracic blood volume changes on steady-state cardiac output. Circ Res 38: 255–261, 1976.Crossref | ISI | Google Scholar4 Rothe C. Point: Active venoconstriction is important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis. J Appl Physiol. In press.Google ScholarjapJ Appl PhysiolJournal of Applied PhysiologyJ Appl Physiol8750-75871522-1601American Physiological SocietyjapJ Appl PhysiolJournal of Applied PhysiologyJ Appl Physiol8750-75871522-1601American Physiological SocietyjapJ Appl PhysiolJournal of Applied PhysiologyJ Appl Physiol8750-75871522-1601American Physiological SocietyjapJ Appl PhysiolJournal of Applied PhysiologyJ Appl Physiol8750-75871522-1601American Physiological SocietyJohn V. Tyberg, University of CalgaryMichael K. Stickland, and University of WisconsinVincent J. B. RobinsonMedical College of GeorgiaOctober2006Loring B. RowellUniversity of WashingtonOctober2006Erik Sandblom, Michael Axelsson, and Anthony P. FarrellGöteborg UniversityOctober2006Artin A. ShoukasThe Johns Hopkins University School of MedicineOctober2006To the Editor: The authors (2a, 4) agree that veins can contract actively and they differ only with respect to how important this mechanism is in exercise and orthostasis. We believe that active venoconstriction is even more important than Dr. Rothe has suggested.Even moderate mental stress reduces the capacitance of the forearm by ∼10% (3). If serial subtraction reduces forearm venous unstressed volume by 10%, it is very likely that the sympathoexcitation of exercise would reduce unstressed volume at least as much and that other vascular beds would also be involved.Flamm et al. (2) documented the redistribution of blood volume during bicycle exercise, as noted by Rothe (4). The spleen decreased its volume by almost 50% and the heart increased its volume by 80% at peak exercise. Such a redistribution is unequivocally important.In a modeling study (1), we demonstrated that only decreases in venous unstressed volume (15–20%) were effective in raising LVEDP to substantial levels (∼25 mmHg); decreases in contractility and increases in peripheral resistance were not effective.Finally, we suggest that changes in venous capacitance can be much more readily appreciated by the use of pressure-volume plots (5)—such studies need not be particularly invasive (3)—rather than pressure-flow plots (e.g., right atrial pressure vs. venous return). In the past, ambiguities in the concept of venous return (i.e., blood volume redistribution and/or instantaneous caval flow rate) may have obscured how venoconstriction increases end-diastolic volume and stroke volume and, thereby, modulates cardiac output (5) during exercise and orthostasis. To the Editor: During orthostasis, Pra falls to zero: cardiac output (CO), EDV, SV fall despite extensive vasoconstriction and, probably, hepatic venoconstriction (2a, 3). MAP is maintained until progressive rise in leg venous volume (viscoelastic creep) causes hypotension—prevented only by muscle contraction (1). Muscle veins lack noradrenergic innervation (Ref. 143 in Ref. 4). Human cutaneous veins constrict significantly when skin and core temperatures fall during heat stress (4, Fig. 30), translocating centrally large volumes that suddenly raise Pra, SV, and thoracic volume (4, Fig. 35). Such unambiguous effects of venoconstriction are not normally seen in exercise (without heating) nor orthostasis. Guyton (2) demonstrated that muscle pumping prevented reductions in Pra normally attending increases in CO at rest (see Ref. 5). Rothe's concept (3) of unstressed venous volume (a virtual volume calculated from a virtual pressure [Pmcf (3)—both unmeasurable], is inadequate when muscle pumping reduces a major compartment volume. Rothe's counter to criticism that resistance increase in constricting veins would elevate pressures in compliant venules upstream is that resistance of the constricting elements is small. But the effect of constriction on their resistance (radius 4) is far greater than on their volume (radius 2). Both debaters' (2a, 3) conclusions that hepatic venoconstriction attends both stresses but that most venous volume is mobilized passively, are supported. However, in autonomically blocked dogs, normal rises in Pra and CO with exercise reveal that muscle pumping translocates enough blood volume centrally to suggest small importance of venoconstriction in exercise as well as orthostasis (5). Finally, Hainsworth's comment (2a) that it is “not possible to obtain accurate quantitative data from humans” overlooks precise measurements of CO, organ blood flow, intravascular pressures, etc., from humans whose orthostatic problems are unique.To the Editor: We appreciate the opportunity to comment on the current discussion regarding the importance of active venoconstriction (1, 2). While we agree with Rothe's general conclusions, we believe his opening sentence gives the impression that active venoconstriction only has evolved in animals that experience gravitational orthostasis (2). This may lead to unnecessary confusion.As comparative cardiovascular physiologists, our interest in the evolution of cardiovascular systems in different animal groups has led us to recently study the role of the venous system in the overall hemodynamics of fish. Fish live in a medium with a density similar to their body fluids and therefore represent vertebrates that evolved and remain in a nearly gravity-free environment where orthostatic blood pooling is infinitesimally small. Research on fish clearly demonstrates that active venous control is an evolutionary ancient trait that evolved well before vertebrates inhabited land and became subjected to strong gravitational forces (2–5).We have found that cardiac preload increases while venous capacitance decreases (as judged by decreased USBV and/or increased MCFP) during exercise (4), environmental hypoxia (2), and after injection of α-adrenergic agonists (3, 5). α-Adrenergic blockade fully or partially abolishes these responses and impairs the ability to increase cardiac stroke volume and output during exercise.Thus active venoconstriction is an integrated and important component during various cardiovascular responses to increase or maintain stroke volume, even in vertebrates as ancient as sharks. Therefore, gravitational forces were at best a secondary selection pressure for the evolution of active venoconstriction.To the Editor: It appears that there still is some controversy (1a, 2) concerning the role of the baroreceptor reflex system in controlling venous capacity and consequently cardiac output. Greene (1) measured the changes in vascular capacitance, resistance, the venous return curve, and cardiac function curve concurrently. They concluded that changes in vascular capacity are the primary mechanism responsible for changes in cardiac output by the reflex system. This change was ∼40%, a value slightly less than reported by Shoukas (3) of 60%. The controversy today seems to be a quantitative one, namely, how important is a 40–60% change in cardiac output mediated by changes in venous capacitance. In exercise where cardiac output changes by as much as 500%, the importance of neurally mediated capacitance changes is most probably minimum and passive changes of blood flow redistribution and the muscle blood pump are extremely important. However, for the elderly suffering from orthostatic intolerance or astronauts returning from a microgravity to a gravity environment, it may be the most critically important mechanism in maintaining cardiac output and arterial pressure. It may be the appropriate time to have another symposium on vascular capacitance.REFERENCES1. Burkhoff D, Tyberg JV. Why does pulmonary venous pressure rise after onset of LV dysfunction: a theoretical analysis. Am J Physiol Heart Circ Physiol 265: H1819–H1828, 1993. Link | ISI | Google Scholar2. Flamm SD, Taki J, Moore R, Lewis SF, Keech F, Maltais F, Ahmad M, Callahan R, Dragotakes S, Alpert N, and et al. Redistribution of regional and organ blood volume and effect on cardiac function in relation to upright exercise intensity in healthy human subjects. Circulation 81: 1550–1559, 1990. Crossref | PubMed | ISI | Google Scholar2a. Hainsworth R and Drinkhill M. Counterpoint: Active venoconstriction is not important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis. J Appl Physiol. In press. Google Scholar3. Robinson VJ, Manyari DE, Tyberg JV, Fick GH, and Smith ER. Volume-pressure analysis of reflex changes in forearm venous function. A method by mental arithmetic stress and radionuclide plethysmography. Circulation 80: 99–105, 1989. Crossref | PubMed | ISI | Google Scholar4. Roth C. Point: Active venoconstriction is important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis. J Apl Physiol. In press. Google Scholar5. Tyberg JV. How changes in venous capacitance modulate cardiac output. Pflugers Arch 445: 10–17, 2002. Crossref | PubMed | ISI | Google ScholarREFERENCES1. Amberson WR. Physiologic adjustments to the standing posture. Univ Med Sch Med Bull 27: 127–145, 1943. Google Scholar1a. Hainsworth R and Drinkhill M. Counterpoint: Active venoconstriction is not important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis. J Appl Physiol. In press. Google Scholar2. Guyton AC, Douglas BH, Langston JB, and Richardson TQ. Instantaneous increase in mean circulatory pressure and cardiac output at onset of muscular activity. Circ Res 11: 431–441, 1962. Crossref | PubMed | ISI | Google Scholar3. Rothe C. Point: Active venoconstriction is important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis. J Appl Physiol. In press. Google Scholar4. Rowell LB. Cardiovascular adjustments to thermal stress. In: Handbook of Physiology. The Cardiovascular System: Peripheral Circulation and Organ Blood Flow. Bethesda, MD: Am Physiol Soc, sect 2, vol III, part 2. Google Scholar5. Sheriff DD, Rowell LB, and Scher AM. Is rapid rise in vascular conductance at onset of dynamic exercise due to muscle pump. Am J Physiol Heart Circ Physiol 265: 1227–1234, 1993. Link | ISI | Google ScholarREFERENCES1. Hainsworth R and Drinkhill M. Counterpoint: Active venoconstriction is not important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis. J Apl Physiol. In press. Google Scholar2. Rothe C. Point: Active venoconstriction is important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis. J Appl Physiol. In press. Google Scholar2. Sandblom E and Axelsson M. Adrenergic control of venous capacitance during moderate hypoxia in the rainbow trout (Oncorhynchus mykiss): the role of neural and circulating catecholamines. Am J Physiol. In press. Google Scholar3. Sandblom E, Axelsson M, and Farrell AP. Central venous pressure and mean circulatory filling pressure in the dogfish, Squalus acanthias: adrenergic control and the role of the pericardium. Am J Physiol. In press. Google Scholar4. Sandblom E, Farrell AP, Altimiras J, Axelsson M, and Claireaux G. Cardiac preload and venous return in swimming sea bass (Dicentrarchus labrax L.). J Exp Biol 208: 1927–1935, 2005. Crossref | PubMed | ISI | Google Scholar5. Zhang Y, Weaver L Jr, Ibeawuchi A, and Olson KR. Catecholaminergic regulation of venous function in the rainbow trout. Am J Physiol Regul Integr Comp Physiol 274: R1195–R1202, 1998. Link | ISI | Google ScholarREFERENCES1. Greene AS and Shoukas AA. Changes in canine cardiac function and venous return curves by the carotid baroreflex. Am J Physiol Heart Circ Physiol 251: H288–H296, 1986. Link | ISI | Google Scholar1a. Hainsworth R and Drinkhill M. Counterpoint: Active venoconstriction is not important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis. J Appl Physiol. In press. Google Scholar2. Rothe C. Point: Active venoconstriction is important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis. J Appl Physiol. In press. Google Scholar3. Shoukas AA and Sagawa K. Control of total systemic vascular capacity by the carotid sinus baroreceptor reflex. Circ Res 33: 22–33, 1973. Crossref | PubMed | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation Related ArticlesCORRIGENDUM 01 Dec 2006Journal of Applied PhysiologyCited ByUnderstanding Guyton's venous return curvesDaniel A. Beard, and Eric O. Feigl1 September 2011 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 301, No. 3The venous circulation: A piscine perspectiveComparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, Vol. 148, No. 4Commentary on Viewpoint “Human experimentation: No accurate, quantitative data?”Carl F. Rothe1 March 2007 | Journal of Applied Physiology, Vol. 102, No. 3 More from this issue > Volume 101Issue 4October 2006Pages 1267-1268 Copyright & PermissionsCopyright © 2006 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00794.2006PubMed16973821History Published online 1 October 2006 Published in print 1 October 2006 Metrics" @default.
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