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POINT-COUNTERPOINT
Department Cellular and Integrative Physiology
Indiana University School of Medicine
Indianapolis, Indiana
e-mail: crothe{at}iupui.edu
ABSTRACT
PURPOSE AND SCOPE OF THE POINT:COUNTERPOINT DEBATES: This series of debates was initiated for the Journal of Applied Physiology because we believe an important means of searching for truth is through debate where contradictory viewpoints are put forward. This dialectic process whereby a thesis is advanced, then opposed by an antithesis, with a synthesis subsequently arrived at, is a powerful and often entertaining method for gaining knowledge and for understanding the source of a controversy.
Before reading these Point:Counterpoint manuscripts or preparing a brief commentary on the content, the reader should understand that authors on each side of the debate are expected to advance a polarized viewpoint and to select the most convincing data to support their position. This approach differs markedly from the review article where the reader expects the author to present balanced coverage of the topic. Each of the authors has been strictly limited in the lengths of both the manuscript (1,200 words) and the rebuttal (400). The number of references to publications is also limited to 30, and citation of unpublished findings is prohibited.
We bipeds, who tend to pool blood in our lower body and legs while standing (orthostatic hypotension), have evolved "active venoconstriction." During severe exercise, venoconstriction is also important for maintaining or increasing the end-diastolic volume (EDV). Experimental proof of active venoconstriction in humans is sparse, because conclusive evidence requires major invasive techniques.
Venoconstriction reduces the venous unstressed volume. From a plot of the venous volume-to-pressure relationship (V/P)—the capacitance—this unstressed volume is a virtual volume computed by extrapolating a linear portion of the capacitance relationship over the normal operating range to zero transmural pressure (see Fig. 1) It cannot be directly measured, but it is defined as the difference between the total contained volume—the capacity—and the stressed volume, which is the product of the compliance and pressure at a specific transmural pressure (14). Active venoconstriction results from activation of the vascular contractile elements, such as smooth muscle. Passive reduction in venous volume results from a decrease in distending pressure. A mathematical model explains these relationships (16).
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30% of the total blood volume is in the stressed volume compartments (Ref. 15, page 1295). In humans, the liver is the most important controllable blood reservoir in the body, and the "control of hepatic capacitance could well have a pivotal role in cardiovascular homeostasis, particularly during exercise and orthostatic stress" (Ref. 13, page 521). The mean circulatory pressure (Pmcf) is the equilibrium pressure if the blood flow is zero and the blood volume is redistributed so that the pressures are equal throughout the body before any reflex compensation (7–9, 14). By definition of compliance, the Pmcf is the ratio of the total stressed volume in the body to the total vascular compliance. Thus the total unstressed volume equals the total circulating blood volume minus the product of total vascular compliance times the Pmcf (14).
Guyton and Hall (6) have stated "Note that at a blood volume of about 4000 ml the mean circulatory pressure is close to zero because this is the ‘unstressed volume’ of the circulation, but at a volume of 5000 ml, the filling pressure is the normal value of 7 mm Hg. Similarly, at still higher volumes, the mean circulatory filling pressure increases almost linearly." Maximal sympathetic stimulation increases the Pmcf from 7 mmHg to 17 mmHg and reduces the unstressed by 600 ml, whereas complete inhibition of the sympathetic nervous system reduces the Pmcf to 4 mmHg and increases the total stressed volume by 350 ml (Ref. 6, page 239–240 and Fig. 20–10).
An adequate cardiac output is a sine qua non for survival during severe stress. However, an increase in cardiac contractility can only reduce the ESV from a normal ejection fraction (SV/EDV) of 0.70 to 1. Furthermore, at high HR, the EDV is limited, because the duration of systole then greatly limits the time available for filling. Thus, maintaining the EDV in orthostatic hypotension, and increasing the EDV in exercise, is crucial. Enhanced atrial contraction aids diastolic filling, as does the skeletal muscle pump while running. Redistribution of the blood volume (16) is also important.
Whereas the normal cardiac output is 5 l/min with a heart rate of 72 beats/min and a stroke volume of 69 ml, well-trained athletes can attain a maximum cardiac output of 36.0 ± 1.6 l/min with a heart rate of 190 ± 3.6 beats/min and a stroke volume of 189 ± 6.6 ml (3). Pentathletes on a treadmill and using 99mTc ventriculography, showed a significantly increased EDV and decreased ESV (22). Human subjects on a bicycle at maximal oxygen update showed a 10% increase EDV and a 19% decrease in abdominal blood volume measured via 99mTc-labeled erythrocytes (4). Hainsworth (12) concluded that humans do not have a large spleen and so are unlikely to mobilize more than 5 ml/kg to lead to increase cardiac output by 50%. However, this amount "may be sufficient to maintain cardiac output in an adequate although reduced level in the upright position" (page 254). See also Ref. 11.
Shoukas and Sagawa (24) provided evidence of active venoconstriction during changes in carotid sinus pressure (ISP). The total blood volume shift from the body was 7.5 ml/kg from changing carotid sinus pressure between 75 and 200 mmHg. Because changes in ISP did not significantly change vascular compliances, they concluded that the blood came from the unstressed volume and that a 25 mmHg change in ISP can cause a 30–40% change in cardiac output via venoconstriction. In another study using constant perfusion, changing carotid sinus pressures between 50 and 200 mmHg caused a 4.7 ml/kg change in splanchnic volume. They concluded that the splanchnic vascular bed contributes a major part of the blood mobilized by the carotid sinus reflex (1).
In the second edition on Human Cardiovascular Control, Rowell (21) devoted four chapters to the problems of orthostatic hypotension in humans. We agree (Rowell's pages 72–73) that passive elastic recoil of the venous bed related to the reduction in cardiac output is somewhat more important than active venoconstriction (18).
In another dog study, extrapolating the data to zero Pmcf required a hemorrhage, before reflex activity could occur, of 17 ml/kg body wt (18% of the total blood volume). With reflexes intact, the hemorrhage to reduce the Pmcf to zero was 25 ml/kg, by 2 min. The difference (8 ml/kg) estimates the magnitude of venoconstriction (2).
Rowell (21, pages 73–74) claimed that active venoconstriction, causing a reduction in volume, will simultaneously cause a proportionally much larger change in resistance to flow. This will cause a passive increase in upstream pressure and distended volume if the inflow does not decrease. However, whereas the vasculature as a whole may be highly compliant, the compliance of the capillaries and venules, because of their extremely small size and collagen fiber walls, may be relatively noncompliant (10, 23). Because of the huge number of venules and small veins and huge total cross-sectional area, the resistance is minute (17). To measure liver volume changes in response to norepinephrine infused via the portal vein at 8 µg·min-1·kg body wt–1, Rothe and Maass-Moreno (19) used servo-null micropipettes to measure the pressure in 50-µm diameter hepatic venules of anesthetized rabbits. They measured lobe thickness to estimate liver volume changes (5) and used an ultrasound flow probe to measure total hepatic blood inflow. The liver volume decreased 8%. The norepinephrine, which was not fully extracted by the liver, caused the systemic arterial pressure to increase 23%. Heart rate decrease 8%, portal venous pressure increased 3.4 mmHg, and hepatic flow increased 2%. The hepatic venule pressure, just downstream from the hepatic sinusoids, significantly increased 1.6 mmHg. Because the liver lobe thickness decreased significantly although hepatic flow and hepatic venular pressure increased, they concluded that norepinephrine causes active venoconstriction of the hepatic capacitance vessels (19, 20).
In conclusion, active venoconstriction provides a rapid, self-contained blood transfusion to the stressed volume in exercise and orthostasis.
REFERENCES
This article has been cited by other articles:
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  C. F. Rothe Commentary on Viewpoint "Human experimentation: No accurate, quantitative data?" J Appl Physiol, March 1, 2007; 102(3): 1289 - 1289. [Full Text] [PDF]
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D. D. Sheriff, R. A. Augustyniak, and D. S. O'Leary Active venoconstriction is/is not important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis J Appl Physiol, November 1, 2006; 101(5): 1531 - 1531. [Full Text] [PDF]
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