DSc (Fisiologie), North-West University, Potchefstroom CampusIn this study use was made of volume expansion with dextran on sheep
with normal hearts and with cardiac failure in order to examine the
mechanisms which are important in the control of the relation of the
cardiopulmonary blood volume to stroke volume as well as to establish
whether these mechanisms play a role in the overall hemodynamic control.
A Swan-Ganz catheter was used for right heart catheterisation to establish pulmonary pressures and to establish the cardiac output after
a cold five per cent dextrose injection was made. A radio-cardiogram
was obtained by the injection of 1-5m Ci technetiumpertechnetate
into the right atrium and the measuring of its activity with an Nal
crystal. At the time the radio-cardiogram was taken an ECG was registered from which the cardio pulmonary flow index was calculated. The
cardiopulmonary blood volume was calculated as the product of the
cardiopulmonary flow index and the stroke volume.
A cardiopulmonary flow index which under normal physiological conditions vary between five and 8,5 can be assumed as relative constant,
if compared with changes from a control value of seven to values of
28 found with heart failure in sheep with gousiekte.
The mean pulmonary intravascular pressure (approximate transmural
pressure) is not homogeneous throughout the pulmonary circulation,
because changes in the intrapleural pressure were not taken in account.
In spite of this the approach of Oakley et al. ( 1962) and others were
used in this study to show in vivo changes in pulmonary vasoactivity.
Changes in pulmonary vasoactivity were established through changes
in the cardiopulmonary blood volume and the mean pulmonary intravascular pressure (approximate transmural pressure). An increase in
the cardiopulmonary blood volume and the mean pulmonary intravascular
pressure indicates a passive pulmonary vasodilation and a decrease
in the cardiopulmonary blood volume and increase in the mean pulmonary
intravascular pressure indicate an active pulmonary vasoconstriction.
This method is more suitable for the lung circulation than the measurement of resistance for the observance of changes in vasoactivity.
The observance of vasoactivity in the lungs coupes great experimental
and physiological problems because active and passive processes function in the pulmonary circulation. Sometimes these active and passive
processes take place simultaneously and the more powerful dominates .
In spite of this the in vivo method for the measurement of pulmonary
vasoactivity is accompanied by great advantages over the in vitro
methods because no nerve supply exists in the isolated specimen and
manifestations like damage or unintensional rubbing of the vascular
endothelium hamper the interpretation of results.
It was pointed out that in the case of sheep with low initial heart
rates active vasoconstriction of the pulmonary vessels take place
after volume expansion in order to maintain the relation between the
cardiopulmonary blood volume and the stroke volume at a value of about
seven for normal hearts. Because the Bainbridge reflex also functions
in the experimental animals with low initial heart rates, the active
vasoconstriction apparently, and probably additionally functions
in conjunct ion with the Bainbridge reflex. Another mechanism, the
Starling mechanism, on the other hand functions in the case of high
initial heart rates to maintain the relation of the cardiopulmonary
blood volume to stroke volume . In the case of sheep with cardiac
failure the different mechanisms do not function effectively and the
cardiopulmonary flow index rises very steeply. A resting heart rate
of 80 beats/min must not be seen as the approximate value for active
pulmonary vasoconstriction to occur, whereas the resting heart rates
may vary from sheep to sheep and as a consequence may show a spread
in results. This study lends itself to statistical analysis of groups
of experimental animals and not to an analysis of data from individual
animals.
With blocking receptors the problem arises that antagonists are not
fully selective and it is uncertain whether receptors are fully blocked
before an experiment. In spite of this problem agonists were injected
intravenously to deter mine the extent of blockage before volume expansion. With the aid of blocking receptors it was shown that the active
vasoconstriction functions via a parasympathetic efferent mechanism.
The receptors which initiate this active vasoconstriction are probably
seated in the walls of the pulmonary arteries and are probably dependent on the changes in pulmonary pressure and not on the absolute
pressure
It has been shown that the relation of the cardiopulmonary blood volume
to stroke volume is not dependent upon the preload of the heart and
relatively independent from the after-load of the heart when mean arterial pressures are lower than about 140nm Hg. The cardiopulmonary
flow index can therefore be regarded as a good index to describe the
pumping ability of the heart. The constancy of the cardiopulmonary
flow index within the normal physiological range of five to 8,5 and
the large increases in the cardiopulmonary flow index found in the
event of cardiac failure, make it a good noninvasive criterion which
in future can have certain diagnostic applications in veterinary science
and medicine. From a physiological point of view this project yields
more quantitative data regarding pulmonary reflexes and it has lent
meaning to a mechanism which together with the Bainbridge and the
Starling mechanism can possibly play an important role in hemodynami c
control.
With studying the relation of the cardiopulmonary blood volume to
stroke volume, this project yields more quantitative data regarding
the importance of in vivo control of the different volumes concerned,
as well as the role of the different volumes in the overall hemodynamic
control.Doctora
