Download claim a 3 ml/kg change in effective circulatory volume (the total

Point:Counterpoint
1266
REFERENCES
1. Brunner MJ, Shoukas AA, and MacAnespie CL. The effect of the
carotid sinus baroreceptor reflex on blood flow and volume redistribution in
the total systemic vascular bed of the dog. Circ Res 48: 274 –285, 1981.
2. Hainsworth R and Drinkhill MJ. Counterpoint: Active venoconstriction
is not an important adjunct to maintaining or raising end-diastolic volume
and stroke volume during exercise and orthostasis. J Appl Physiol. In Press.
3. Herndon CW and Sagawa K. Combined effects of aortic and right atrial
pressure on aortic flow. Am J Physiol 217: 65–72, 1969.
4. Karim F and Hainsworth R. Responses of abdominal vascular capacitance to stimulation of splanchnic nerves. Am J Physiol 231: 434 – 440,
1976.
5. Noble BJ, Drinkhill MJ, Myers DS, and Hainsworth R. Reflex control of
splanchnic blood volume in anesthetized dogs. J Physiol 513: 363–272,
1998.
6. Rothe CF, Johns BL, and Bennett TD. Vascular capacitance of dog
intestine using mean transit time of indicator. Am J Physiol Heart Circ
Physiol 234: H7–H13, 1978.
7. Sheriff D. Point: The muscle pump raises muscle blood flow during
locomotion. J Appl Physiol 99: 371–372, 2005.
8. Shoukas AA, MacAnespie CL, Brunner L, and Watermeier MJ. The
importance of the spleen in blood volume shifts of the systemic vascular
bed caused by the carotid sinus baroreceptor reflex in the dog. Circ Res 49:
759 –766, 1981.
REBUTTAL FROM DRS. HAINSWORTH AND DRINKHILL
The main difference between Rothe’s and our points of view
seems to be in the extent to which we regard the likely effect
J Appl Physiol • VOL
of the reduction in capacitance caused by venous constriction
in humans to be of physiological importance. We both agree
that veins are the major reservoir of blood and that passive
changes in volume, caused by external compression or by
changes in flow into them, are probably more important than
changes due to venoconstriction. We also agree that, in humans, it is likely that it is the liver that forms the major active
reservoir. There is, however, a statement at the start of Rothe’s
article that we would question. He states that “we
bipeds. . . .have evolved active venoconstriction.” This may be
so, but, as he points out in the same paragraph, “proof of active
venoconstriction in humans is sparse.” This really is the nub of
the problem. A major limitation to our knowledge of the
importance of active venoconstriction in humans is that virtually all the research has been done in animals, mainly dogs (2,
3). In dogs, the largest controllable reservoir is the spleen and
this is very much smaller in humans. In absence of evidence to
the contrary, we have worked on the assumption that humans
behave in the same way as splenectomized dogs, and this leads
us to the conclusion that active venoconstriction is unlikely to
be of major physiological importance (4, 5). In addition, we
know that active venoconstriction occurs at low levels of
sympathetic activity (6), which would suggest that, in supine
resting humans, 50% of the response would already be engaged
(1), leaving little reserve. However, if Rothe is correct and
humans have indeed evolved differently from dogs, to facilitate
maintenance of their upright posture, active venoconstriction
could be of more importance. The problem, however, is that at
present there is no evidence for this and until such evidence is
forthcoming we feel we have to hold to the view that active
venoconstriction is unlikely to have a major role in cardiovascular control.
REFERENCES
1. Graham LN, Smith PA, Huggett RJ, Stoker JB, Mackintosh AF, and
Mary DASG. Sympathetic drive in anterior and inferior uncomplicated
acute myocardial infarction. Circulation: 109: 2285–2289, 2004.
2. Hainsworth R and Karim F. Responses of abdominal vascular capacitance in the anaesthetized dog to changes in carotid sinus pressure.
J Physiol 262: 659 – 677, 1976.
3. Karim F and Hainsworth R. Responses of abdominal vascular capacitance to stimulation of splanchnic nerves. Am J Physiol 231: 434 – 440,
1976.
4. Noble BJ, Drinkhill MJ, Myers DS, and Hainsworth R. Reflex control of
splanchnic blood volume in anaesthetized dogs. J Physiol 513.1: 263–272,
1998.
5. Noble BJ, Drinkhill MJ, Myers DS, and Hainsworth R. Blood mobilization from the liver of the anaesthetized dog. Expt Physiol 83: 513–522,
1998.
6. Noble BJ, Drinkhill MJ, Myers DS, and Hainsworth R. Mechanisms
responsible for changes in abdominal vascular volume during sympathetic
nerve stimulation in anaesthetized dogs. Expt Physiol 82: 925–934, 1997.
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claim a 3 ml/kg change in effective circulatory volume (the
total stressed volume) of the liver and intestinal bed. In conjunction with a total body compliance of 2.5
ml䡠kg⫺1 䡠mmHg⫺1, this would change the Pmcf by 1.2 mmHg.
Assuming that the Pra at equilibrium would be increased by the
same amount, they then claim, using “Guyton’s curves,” that
this would increase the cardiac output by only 20%. Herndon
and Sagawa (Ref. 3, Fig. 7) suggest that the sensitivity of
cardiac output to changes in Pra is 52 ml䡠min⫺1 䡠kg⫺1 change
in flow per millimeter mercury change in Pra. Thus a change in
cardiac output from a 1.2 mmHg change in Pra would be a
much larger increase of 60 ml䡠min⫺1 䡠kg⫺1. Other studies have
reported much larger active venous changes than the 3 ml/kg.
For example, for dogs, carotid baroreceptor changes, a 7.0
ml/kg change (1); maximum sympathetic simulation, with
spleen intact 7.2 ml/kg, without spleen 4.3 ml/kg (4); carotid
sinus pressure changes, with spleen 8.4 ml/kg, without spleen
7.2 ml/kg (8).
They also claim (Ref. 2; Fig. 2) that the intestinal bed
provides a negligible active venoconstriction response based
on the data from the study by Noble et al. (4). We (6) evaluated
active and passive venoconstriction in segments of dog jejunum. Norepinephrine caused an active change in intestinal
blood volume of 24% and a passive change of 62%. Active
venoconstriction is important.