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Why relate venoconstriction to end-diastolic volume or stroke volume?
What's the (counter)point?
Active venoconstriction -- even more important in regulating end-diastolic volume / stroke volume?
Passive volume mobilization dominates.
Active venoconstriction: its evolutionary roots clarified?
This is a Quantitative Issue
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sheldon magder, professor mcgill university
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sheldon.magder{at}muhc.mcgill.ca sheldon magder
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The point:counterpoint “Active venoconstriction is/is not important in maintaining or raising end-diastolic volume and stroke volume during exercise” was very informative and reflects the expertise of the protagonists. However, I have a problem with the question. During exercise, cardiac output increases in linear proportion to oxygen consumption (4) and heart rate increases according to the relative workload (1) which suggests that these two variables are the controlled ones. Since cardiac output is the product of heart rate and stroke volume, the stroke volume and EDV must be dependent variables. Thus changes in capacitance should be related to cardiac output and not stroke volume. We found that in response to a decrease in carotid sinus pressure, the baroreceptor reflex defended a fall in blood pressure by a recruitment of around 10 ml/kg from the splanchnic bed even with a rise in arterial pressure and an increase in the fraction of flow to the splanchnic region(2), which argues against a purely passive effect. We also surprisingly found that the venous resistance draining the splanchnic region decreased at the same time as the arterial resistance increased(2). A similar decrease in splanchnic capacitance occurred with heat stress but without a change in venous resistance(3). Both authors in this point:counterpoint fail to account for how the high cardiac output that occurs during exercise is achieved. In a theoretical analysis we concluded that recruitment of unstressed volume in combination with redistribution of blood flow to muscles and decreased venous resistance of muscle and splanchnic beds are required to obtain the high cardiac output(5). Recruitment of unstressed volume alone would result in very high capillary pressures and likely excessive capillary filtration. Reference List 1. Clausen JP. Circulatory adjustments to dynamic exercise and effect of physical training in normal subjects and in patients with coronary artery disease. Progress in Cardiovascular Diseases 18: 459-495, 1976. 2. Deschamps A and Magder S. Baroreflex control of regional capacitance and blood flow distribution with or without alpha adrenergic blockade. J Appl Physiol 263: H1755-H1763, 1992. 3. Deschamps A and Magder S. Effects of heat stress on vascular capacitance. Am J Physiol 266: H2122-H2129, 1994. 4. Ekelund LG and Holmgren A. Central hemodynamics during exercise. Circ Res 20: I-33-I-43, 1967. 5. Magder S. Theoretical analysis of the non-cardiac limits to maximum exercise. Can J Physiol and Pharmacol 80: 971-979, 2002. |
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Wayne Mitzner, Professor Johns Hopkins University
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wmitzner{at}jhsph.edu Wayne Mitzner
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The underlying issue being discussed (4) seems much broader than the 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 4 or 5 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. Since it is axiomatic that the heart can’t 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 doesn’t 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. References: 1. 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. 2. Mitzner W and Goldberg H. The effect of epinephrine on the resistive and compliant proeprties of the canine systemic vasculature. Journal of Applied Physiology 39: 272-280, 1975. 3. Mitzner W, Goldberg H, and Lichtenstein S. Effect of thoracic blood volume changes on steady-state cardiac output. Circulatory Research 38: 255-261, 1976. 4. Rothe C, Hainsworth R, and Drinkhill M. Point:Counterpoint: Active venoconstriction is / is not important in maintaining or raising end- diastolic volume and stroke volume during exercise and orthostasis. J Appl Physiol 101: xxx-xxx, 2006. |
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John V. Tyberg, Professor University of Calgary, Michael K. Stickland, Vincent J. B. Robinson
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jtyberg{at}ucalgary.ca John V. Tyberg, et al.
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The authors(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 mm Hg); 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. John V. Tyberg, MD, PhD University of Calgary Michael K. Stickland, PhD University of Wisconsin Vincent J. B. Robinson, MD Medical College of Georgia REFERENCES 1. Burkhoff D and Tyberg JV. Why does pulmonary venous pressure rise after onset of LV dysfunction: a theoretical analysis. Am J Physiol 265: H1819-1828, 1993. 2. 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. 3. 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. 4. Rothe CF, Hainsworth R, and Drinkhill M. Point-Counterpoint: Active venoconstriction is / is not important in maintaining or raising end- diastolic volume and stroke volume during exercise and orthostasis. J Appl Physiol 101: XXX-XXX, 2006. 5. Tyberg JV. How changes in venous capacitance modulate cardiac output. Pflugers Arch 445: 10-17, 2002. |
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Loring B Rowell University of Washington
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brengelm{at}seanet.com Loring B Rowell
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During orthostasis, Pra falls to zero: cardiac output (CO), EDV, SV fall despite extensive vasoconstriction and, probably, hepatic venoconstriction (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 (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 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 (radius4) is far greater than on their volume (radius2). Both debaters’ (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 (3) that 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. References 1. Amberson WR. Physiologic adjustments to the standing posture. Univ. Md. Sch. Med. Bull. 27:127-145, 1943. 2. 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. 3. Rothe CF, Hainsworth R, and Drinkhill M. Active venoconstriction is/is not important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis. J. Appl. Physiol 101: xxx- xxx, 2006. 4. Rowell LB. Cardiovascular adjustments to thermal stress. In: JT Shepherd, FM Abboud eds. Handbook of Physiology. The Cardiovascular System: Peripheral Circulation and Organ Blood Flow, sect 2, vol III, part 2. 5. 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. Loring B. Rowell, Ph.D. Professor Emeritus Department of Physiology and Biophysics University of Washington Seattle, WA USA |
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Erik Sandblom Göteborg University, Michael Axelsson and Anthony P. Farrell
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erik.sandblom{at}zool.gu.se Erik Sandblom, et al.
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We appreciate the opportunity to comment on the current discussion regarding the importance of active venoconstriction (1). 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 (1). 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 haemodynamics 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 alpha- adrenergic agonists(3, 5). Alpha-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 in order 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. References 1. Rothe CF, Hainsworth R, and Drinkhill MJ. Point:Counterpoint: Active venoconstriction is/is not important in maintaining or raising end- diastolic volume and stroke volume during exercise and orthostasis. J Appl Physiol 101: 2006. 2. 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 2006. 3. 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 2006. 4. 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. 5. Zhang Y, Weaver L, Jr., Ibeawuchi A, and Olson KR. Catecholaminergic regulation of venous function in the rainbow trout. Am J Physiol 274: R1195-1202, 1998. |
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Artin A. Shoukas, Professor The Johns Hopkins Univ. School of Medicine
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ashoukas{at}bme.jhu.edu Artin A. Shoukas
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It appears that their still is some controversy 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 approximately 40%, a value slightly less than reported by Shoukas (2) of 60%. The controversy today seems to be a quantitative one, namely, how important is a 40 to 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 micro gravity 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. 1. A.S. Greene and A. A. Shoukas. Changes in canine cardiac function and venous return curves by the carotid baroreflex. Am J Physiol Heart Circ Physiol,; 251: 288 – 296, 1986 2. Rothe CF, Hainsworth R, and Drinkhill MJ. Point:Counterpoint: Active venoconstriction is/is not important in maintaining or raising end- diastolic volume and stroke volume during exercise and orthostasis. J Appl Physiol 101: 2006. 3. Shoukas, A.A., and K. Sagawa. Control of total systemic vascular capacity by the carotid sinus baroreceptor reflex. Circ Res 33:22 33, 1973 |
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