| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Physiology
Indiana University School of Medicine
Indianapolis, Indiana
e-mail: eroth{at}iupui.edu
To the Editor: Hainsworth and Drinkhill (1) and I (4) agree that active venoconstriction is real and that more research is needed to define its role in humans. I suggest, however, that the sympathetic activity data from humans with acute myocardial infarction (1, 1a) cannot be extrapolated to that for normal humans.
Magder (2) states that cardiac output increases in proportion to oxygen consumption and increased heart rate in accord with the relative workload. I agree with these facts. However, to conclude that cardiac output and heart rate are thus "controlled" variables is not valid. The cardiovascular is a closed loop system in which volume redistribution (via the principle of mass balance) leads to a new equilibrium following a disturbance. With competent valves, the cardiac output (CO) for each ventricle is determined by its heart rate (HR) times [end-diastolic volume (EDV) minus end-systolic volume (ESV)]. The initial influence of an increased stressed volume by active venoconstriction, which reduces the unstressed vascular volume, will be on the EDV. A reduction in ESV, by an increase in cardiac contractility, is also likely. Magder's theoretical analysis (2, 5) of the response of the circulatory system to maximum exercise has the serious flaw of not including the crucially important large (2–4 times) increase in heart rate. A mathematical model that realistically includes the major variables and parameters without being overwhelming (31 ) is essential for clear understanding of these cardiovascular interactions.
Mitzner (2) also believes that active venoconstriction is important, but he criticizes us for not explaining how "cardiac output can rise to four or five times its baseline level." I agree that even a doubling of the stressed blood volume (20 ml/kg) by an active reduction of the unstressed volume is unlikely. Increasing the LV EDV or stroke volume by four times during exercise is most unlikely. However, an increase of heart rate, by three times baseline, is probably the most important of many compensatory mechanisms. Many parameters are changed, including active venoconstriction.
Rowell (2) states that the unstressed venous volume is a virtual volume calculated from a virtual pressure (Pmcf). However, veins do contain volume at zero distending pressure. Furthermore, although the accuracy is not perfect, the Pmcf can be measured and the overall vascular compliance can be reasonably estimated, but not the venous compliance. What we currently cannot measure is the overall peripheral venous distending pressure. I agree that the skeletal muscle pump is important (5), but it alone will not lead to a cardiac output of 25 l/min in exercising humans.
Sandblom (2) provides invaluable information suggesting that active venoconstriction evolved in fish, which live in an environment little influenced by gravity, long before vertebrates inhabited land. The evolutionary pathways must be complex.
In conclusion, active venoconstriction is a minor factor in exercise, but this mechanism for humans is important as a noninvasive, rapidly acting, and effective blood transfer to the active circulating blood volume during cardiovascular stresses, such as standing.
FOOTNOTES
1 An updated Version 5 of the Cardiovascular Interactions Project is available as a Learning Object by C. F. Rothe in the Archive of Teaching Resources 2005, or on a CD by request to the author. 
REFERENCES
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
