Journal of Applied Physiology AJP: Advances in Physiology Education
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J Appl Physiol 102: 1289, 2007; doi:10.1152/japplphysiol.01325.2006
8750-7587/07 $8.00
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LETTER TO THE EDITOR

Commentary on Viewpoint "Human experimentation: No accurate, quantitative data?"

To the Editor: Dr. Rowell (5) provided invaluable information about the control of the cardiovascular system of humans subjected to various stresses. Rowell's example of the difference in blood distribution between dogs and humans while standing in a cold environment and a hot one proves his contention: accurate data are available from humans and extrapolation between species can lead to erroneous conclusions. However, in the debate between Hainsworth and me (1, 3) about the importance of active venoconstriction, the major problem is measuring active changes in peripheral venous unstressed blood volume. For this, no direct and accurate method is currently available for any species. It can only be estimated as the difference between the total compartment volume and its stressed volume. Rowell is confused. My concept of total unstressed volume (see Ref. 3, p. 1262, right column) is not "a virtual volume calculated from a virtual pressure [Pmcf..."] (2). The Pmcf is used to estimate the total stressed volume. It is not a measure of peripheral venous distending pressure. While I appreciate the first paragraph of his SUMMARY, most of Rowell's Viewpoint is about direct vs. indirect methods of measuring flow rather than volume.

To understand the complex interactions between the many parameters of the cardiovascular system, a mathematical model that includes the end-diastolic volume (Starling Law) and end-systolic volume (contractility) of both ventricles, heart rate and the compliance, stressed and total volume of the peripheral circulation, and mass balance for blood distribution (4) is helpful.

FOOTNOTES


Address for reprint requests and other correspondence: C. F. Rothe, Dept. Cellular and Integrative Physiology, Indiana Univ. School of Medicine, Indianapolis, IN 46202 (e-mail: crothe{at}iupui.edu)

REFERENCES

  1. Hainsworth R, Drinkhill MJ. Counterpoint: Active venoconstriction is not important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis. J Appl Physiol 101: 1264–1265, 2006.[Free Full Text]
  2. Mitzner W, Tyberg JV, Stickland MK, Robinson VJB, Rowell LB, Sandblom E, Axelsson M, Farrell AP, Shoukas AA. Response to Point:Counterpoint series: "Active venoconstriction is/is not important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis" J Appl Physiol 101: 1267–1268, 2006.[Free Full Text]
  3. Rothe CF. Point: Active venoconstriction is important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis. J Appl Physiol 101: 1262–1264. 2006.[Abstract/Free Full Text]
  4. Rothe CF. Cardiovascular interactions: A major revision of mating an interactive lab book and mathematical model (Descriptive abstract of APS Archive Additions). Adv Physiol Educ 29: 139–140, 2005.[Abstract/Free Full Text]
  5. Rowell LB. Human experimentation: No accurate, quantitative data? J Appl Physiol. In Press.

Carl F. Rothe
 Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana





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