Download Oxygen Consumption of Arterial Smooth Muscle as a Function of

Oxygen Consumption of Arterial
Smooth Muscle as a Function of Active
Tone and Passive Stretch
By R. L. Kosan, B. Sc, and Alan C. Burton, Ph.D.
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• Previous work by other investigators on
the oxygen consumption of isolated vascular
smooth muscle has dealt with the viability of
the muscle after storage and the effects of age,
hormones, and various substrates on the respiration of normal and diseased arterial muscle.1"11 The fundamental question as to how
much the oxygen consumption increases when
vascular smooth muscle maintains active tension in contraction, as in vasoconstriction, has
received little attention. Changes in the respiration of arterial tissue during action of dilator drugs of the nitrate-nitrite series12 have
been reported. The changes in respiration
with active contraction have been investigated
in some other types of smooth muscle, e.g.,
intestinal,13 stomach14 and uterine13 muscle
but, in no instance that we are aware of, has
this been resported for vascular smooth muscle. This was the primary aim of this research.
Initially we attempted to obtain evidence
from the isolated perfused ear of rabbit, where
vasomotor activity is very marked, and the
degree of active contraction of vascular smooth
muscle may be measured quantitatively.11'
Even with a closed circulatory perfusion system of minimal total volume, the arterial-venous differences from which the oxygen consumption could be calculated were too small
to present sufficient accuracy with the polarographic technique we used. In addition the
respiration of other cellular tissues such as the
skin might be affected by pressor drugs, making it impossible to attribute the total increases
From the Department of Biophysics, Medical
School, University of Western Ontario, London, Ontario, Canada.
Supported by a grant from the Medical Research
Council of Canada.
Accepted for publication July 6, 1965.
Circulation Reiearch, Vol. XVIII, January 1966
in O2 consumption to vascular smooth muscle
alone. The use of segments of arteries of the
muscular type, in a modified Warburg respirometer, appeared to be the best initial approach. Smooth muscle is a large part of the
total weight of arteries and the elastic fibres
which also make up most of the rest of the
weight are acellular and presumably do not
consume oxygen.
Fairly large differences in the values for
resting respiration have been reported by other
investigators. Presumably, unphysiological
conditions usually depress the O-2 consumption. We therefore spent some time modifying
certain parameters (O2 tension, CO2 tension,
stretch, etc.) in the Warburg constant-volume
technique used, so as to obtain the maximal
resting respiration possible, approaching presumably the in vivo value.
Methods
Femoral arteries were isolated from mongrel
dogs anaesthetised with sodium pentobarbital
(30 mg/kg). Lengths of 3.5 cm were obtained
from each leg. These were quickly stripped of
any adventitia and rinsed in buffered Ringerglucose solution to remove any blood present.
Whole segments of 15 mm length were then
stretched and tied on to the annuli of a stainless
steel support (fig. 1), the distance between the
annuli being 18 mm. The annuli were open-ended
with an outside diameter of 3.5 mm for this
series of experiments. Each annulus was 2.5 mm
in length, 1.5 mm of which extended into the
end of the artery segment. In the course of
mounting, the arterial segments were all stretched
to about 40% of their initial excised length, that
is, from 15 to 21 mm to compensate for their
retraction upon excision. Thus the mounted
lengths were close to their in vivo lengths.
Although the outer diameter of the vessel segments varied from 2.0 to 4.2 mm, all were tied
on to the same annuli, having an outside diameter
of 3.5 mm. Thus their mounted circumferences
differed from their initial unmounted values, i.e.,
79
80
KOSAN, BURTON
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FIGURE 1
Upper diagram illustrates a Warburg apparatus modified to measure changes in arterial
diameter. The reaction flasks are shaken in the temperature equilibrated bath of the transparent
plastic tank. The camera (c) records changes in the outer diameter of the artery. Lower
diagram shows stretched artery tied on stainless steel annuli. Both diagrams illustrate the
method of mounting the annuli with arteries to the centre well of the flask.
some were stretched circumferentially more than
others. The mounting increased the diameter of
the vessel segment not only at the annuli, but
also considerably at all points between them. The
support with the mounted artery was then
maneuvered into the flat part of a Warburg reaction vessel where it was fastened horizontally
by means of a screw passing through it into a
stationary stainless steel ring which was forcefitted around the bottom of the centre well of
the flask. Figure 1 shows this, along with a
Warburg thermobarometer reaction vessel, which
was identical to the one described above except
that it contained no arterial segment. In addition
to the artery, of net weight between 70 and 120
mg, with its stainless steel supports, the 15 ml
reaction vessel also contained 4 cc of phosphate-
buffered Ringer-glucose solution. Two stock solutions were prepared and designated A and B,
with compositions respectively in mmoles/liter:
NaCl
K Cl
Na2 HPO4
H, PO4
Mg SO4
Dicalcium edetate (Versenate)
B
Calcium chloride
145.3
5.6
4.2
0.2-0.6
1.2
0.027
2.16
These two stock solutions were kept at 4°C
until required. The buffered Ringer's solution was
then made by mixing eight parts of A with one
part of B. Sufficient phosphoric acid was used in
A to produce a pH of 7.4 when the solutions
Circulation Research, Vol. XVIII, January 1966
OXYGEN CONSUMPTION OF ARTERIAL SMOOTH MUSCLE
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were mixed as specified. No trouble was encountered from precipitation of calcium since the
two solutions were kept separate until required.
The stock solution kept well and maintained the
same pH for several weeks. The edetate was included to chelate trace amounts of heavy metal
which would otherwise catalyze the auto-oxidation of catecholamines which were used to increase the tone of the muscle. D-glucose was
added to the mixed solution just before use to
give a final concentration of 200 mg%. Also 0.1
cc of 20% KOH was added to the centre well to
absorb the CO2 produced, and the flask was then
gassed with 100% oxygen. All measurements were
made at 37°C.
Dry weights of the tissue were determined by
drying segments at 60 °C for 72 hours at which
time no further decrease in weight could be
observed. With the bathing solution of Ringerglucose the oxygen consumption of the tissue was
determined by using the constant-volume Warburg technique.17 Readings were usually taken
every 15 minutes for as long as three hours.
Several experiments were done with a bathing
solution of dog plasma instead of Ringer's solution. Since the retention of oxygen by the plasma
was somewhat pressure dependent (traces of
hemoglobin greatly increase the oxygen capacity),
it was decided to record the changes in the
manometer readings after adjusting to constant
pressure, rather than to constant volume. All
readings here were taken at a pO 2 equal to
atmospheric pressure, and were corrected as usual
for thermopressure variations.
To determine the respiratory quotient (RQ),
experiments in which CO2 was absorbed were
compared with those in which COL, was allowed
to accumulate. Therefore, a few experiments had
to be done to determine whether the oxygen
consumption depended on the experimental CO.j
concentration which varied in the RQ experiments
from 0 to 0.5%. Although the COo concentration
at 0.5% does not approach the physiological
range (5%), it is nevertheless equivalent to the
maximum amount of CO2 which can be produced by 100 mg of arterial tissue in one hour.
Five experiments were done in which the oxygen
consumption of one artery preparation, respiring in a gas of CO2 concentration 0%, was compared with that of a paired arterial segment from
the same dog artery but respiring in an atmosphere with a CO2 concentration of 0.5% (fig.
2). A third flask was used as thermobarometer.
The constant CO2 of 0.5% was obtained by replacing the KOH in the center well with a diethanolamine buffer solution. The latter, by virtue
of its ability to combine reversibly or to dissociate
with COo, maintains a constant CO2 in the liquid
and gaseous phases, the actual value depending
Circulation Research, Vol. XV111, January 1966
81
on the concentration of the buffer components,
the pH and the COo flask constants.17 Readings
were taken after adjusting for constant volume.
The above experiments were done with Ringerglucose as the bathing medium. Experiments
with plasma were not attempted. As shown more
completely below, the oxygen consumption was
essentially independent of the CO2 when the
latter ranged from 0 to 0.5%. Unfortunately,
much higher values of CO2 pressure were not
possible using this special buffer with the present
apparatus.
This being so, the direct method of Warburg
was justified in determining the RQ.17 The oxygen
consumption of one smooth muscle preparation,
determined in the presence of the CO2 produced
by the muscle (no KOH present), was compared
with that of another preparation from the same
dog in the absence of CO2 (KOH present in
center well). Since it was shown by our previous
procedures that the oxygen consumption is essentially the same under these two different experi1.0 h
I
0.5
OL
o
o
g
50
TIME (min)
* * *
. . .
100
OXYGEN = 100%
OXYGEN = 99.5%
CARBON DIOXIDE = 0.5%
FIGURE 2
Effect of 0.5% CO2 on the resting oxygen consumption
is not significantly different statistically from the
oxygen consumption with 0% CO2 (0.05 <P < 0.10).
Segments from the same dog artery were used. Lag in
first part of lower curve is probably due to equilibration of the CO2 from the diethenolamine buffer with
the surrounding liquid and gas.
KOSAN, BURTON
82
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mental conditions, one obtains two equations
with two unknowns, the oxygen consumption and
carbon dioxide production and thus the RQ.
It should be noted that the calculation of
carbon dioxide production is very dependent on
the solubility of CO2 in the bathing solution
used. A large correction had to be made to the
standard solubility of CO2 in unbuffered Ringerglucose solution in order to include the retention
of CO2 by the phosphate buffer. The detailed
calculation will not be given here but the net
result obtained was that, according to the Henderson-Hasselbach equation, at pH 7.4 the effective CO 2 solubility is approximately 11 times the
solubility in Ringer's solution without the buffer
present. The effect of this high effective CO 2
solubility is to increase the CO2 flask constant and
hence the calculated CO 2 production by a factor
of about four times (fig. 3).
In our final experiments, the degree of contraction was estimated by photographing the artery
before and during stimulation. A camera (C in
fig. 1) was mounted below a special Warburg
reaction vessel containing the artery. This Warburg flask, together with its thermobarometer flask
was shaken in a transparent plastic tank containing the temperature regulated water. The shaking
was done by linkage with the original Warburg
apparatus. This is shown in figure 1. Buffered
Ringer-glucose was the only bathing solution
used in this series of experiments. The KOH was
added to the centre well and 0.5 ml of either
norepinephrine (levarterenol bitartrate) or epinephrine HC1 was placed in the flask sidearm.
The final flask concentration with either drug was
5 X 10"7 g base/ml. The whole apparatus was
gassed with 100 % O2.
The oxygen consumption of the resting or relaxed segment, and its resting diameter were both
recorded for about }i to % hour. Then the norepinephrine or epinephrine was tipped in from
the sidearm. After allowing two or three minutes
for temperature re-equilibration, the oxygen and
diameter readings were continued for as long as
the contraction was maintained and usually until
the artery diameter returned to its resting value.
Since the films of the artery could not be developed until after the experiment, readings were
taken usually for about two hours after addition
of the drug since this time proved generally sufficient to enable us to compare the final resting
with the initial resting oxygen consumption.
Results
RESTING O2 CONSUMPTION
With buffered Ringer-glucose solution the
mean Qo,, or Qo., (/-(.liters oxygen consumed
/mg wet~wt/hr) "was 0.61 ±0.04 SEM, 11 determinations. Although the Qo 2 varied considerably from the artery of one dog to that of
another, for any given artery the plot of oxygen consumption in ^liters/mg wet weight
versus time was usually quite linear for as
long as two hours after the initial reading.
The average dry weight of the arteries was
27% ± 1% SEM of their wet weights. The Qo2
on this basis thus equals 2.26 ± 0.13 SEM
//liters/mg dry wt/hr. With dog plasma replacing the Ringer-glucose as the bathing solution, the resting Qo2 was 0.65 ± 0.05 SEM
/uliter/mg wet wt/hr or 2.41 ±0.19 SEM
juliters/mg dry wt/hr (7 determinations).
EFFECT OF CO»
As shown in figure 2 the effect of 0.5% CO a
on the resting oxygen consumption is small.
Using paired arterial segments, i.e., segments
from the same dog artery, the values obtained
for the resting oxygen consumption under the
two conditions are shown in table 1. Statistically, no significant difference exists between the
two means, which differ by less than 4%.
On the basis of the foregoing experiments,
TABLE 1
Effect of CO,, on the Oxygen Consumption
Oxygen consumption, Q o .
Artery
no.
1
2
3
4
5
Mean
in 0% CO 2 , 100% O 2
in
^liter/mg wet wt/hr
0.62
0.57
0.63
0.50
0.68
0.58
0.54
0.64
0.49
0.63
0.58 ± 0.02
0.5% CO2, 99.5% O 2
fiMter/mg wet wt/hr
0.60 ± 0.03
SEM
SEM
0.05 < P < 0.10
Circulation Research, Vol. XVIII, January 1966
83
OXYGEN CONSUMPTION OF ARTERIAL SMOOTH MUSCLE
E 1.0
1.0
E
CO
CO
5
O
LJ
o
UJ
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cr
cr
cr
o
o
100
50
TIME (min)
100
TIME (min)
100
OXYGEN CONSUMPTION
CARBON DIOXIDE PRODUCTION
FIGURE 3
heft: lines show uncorrected experimental manometric readings per mg of arterial tissue.
Right: each value on the uncorrected curves has been multiplied by the appropriate flask
constant (Ko = 1.18 mms, Kco = 4.49 mms).
TABLE 2
Respiratory Quotient of Vascular Smooth Muscle
Os consumption
^liter/mg wet wt/hr
0.58
0.64
0.59
0.66
0.57
COs production
jtliter/mg wet wt/hr
0.59
0.62
0.59
0.65
0.55
RQ = COS/OL.
1.02
0.97
1.00
0.98
0.96
Mean RQ = 0.986 ± 0.01 SEM
A sample calculation of the RQ is given in the
appendix.
we felt justified in using the direct method of
Warburg to determine the RQ. The results of
a typical experiment are shown in figure 3. A
summary of the results of five experiments is
shown in table 2.
Figure 4 shows the results obtained with one
artery which was studied during relaxation for
one-half hour, during which time the rate of
oxygen consumption was steady, and then was
stimulated by the addition of 5 X 10"7 g/ml of
epinephrine. As shown by figure 4 and the
Circulation Research, Vol. XVIII, January 1966
photographs in figure 5, the outer diameter of
the artery decreased almost immediately and
at the end of two to seven minutes the contraction was maximal. The average value of
this maximal contraction amounted to a
change of 9% ± 0.5% SEM of the initial diameter. Simultaneous determinations of the oxygen consumption showed that the latter
increased with the increased degree of contraction of the vascular smooth muscle. In the 20
determinations made, a whole spectrum of
values was obtained for the Qo2, during contraction, the range being from 0.52 to 1.02
yuliter/mg wet wt/hr. The mean of all these
was 0.80 ±0.05 SEM /xliter/mg wet wt/hr,
or about a 30% increase over the relaxed value.
From one-half to one and one-half hours after
stimulation, both the oxygen consumption and
the outer diameter of the artery approached
values closely approximating their original
relaxed values.
In some experiments, norepinephrine was
given first, in others, later. The changes in
KOSAN, BURTON
84
zo
OXYGEN CONSUMPTION
DIAMETER CHANGE
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0
100
150
TIME (min)
FIGURE 4
Adrenaline (epinephrine; final flask concentration 5 X 10~7 g/ml) was added at the arrow. Its
effect, in this case, was to decrease the artery diameter by about 9% and to increase the oxygen
consumption over the same period by about 25%. Both diameter and oxygen consumption
eventually approached their initial values.
diameter and 0- consumption were comparable whatever the sequence. The effects of
norepinephrine disappeared more rapidly than
those of epinephrine, and it was extremely
difficult to maintain a contraction for more
than 10 to 20 minutes, with the result that the
number of readings and hence the permissible
accuracy were reduced considerably. Thus,
most of the experiments were done using
epinephrine rather than norepinephrine. Figure 6 summarizes all the results obtained from
the experiments using epinephrine.
Discussion
The average value obtained for the arterial
muscle Qo« of 0.6 /u,liter/mg wet wt/hr (range
0.49 to 0.71) in buffered Ringer-glucose is
somewhat higher than those obtained by previous investigators, whose values have ranged
from 0.1 to 0.5 /iliter/mg wet wt/hr using for
the most part isolated aortic strips. It is to be
expected that on a weight basis the Q0o val-
ues for the femoral artery would be greater
than those of aortic strip due to the considerably smaller amount of nonrespiring elastic
tissue in the media of the femoral artery compared with that in the aorta. On the other hand
our Qoo values exceed even those obtained
recently with a Cartesian diver microrespirometer by Howard et al., who found that the
Qo,, of mesenteric arterioles less than 150 JJL
in diameter averaged 1.05 //.liter/mg dry wt/
hr.
Since no significant correlation was found
between the thickness of the arterial wall in
the segments (thickness varied from 0.15 to
0.3 mm) and the Qo.,, it is probable that the
arterial respiration was not limited significantly by the diffusion of its oxygen supply. The
average value obtained for the resting Qo2 in
plasma, although a little higher than that in
Ringer-glucose is not significantly higher. Also,
as indicated by the RQ value of 0.99 of the
arterial muscle in Ringer-glucose solution, it is
Circulation Research, Vol. XVIII, January 1966
OXYGEN CONSUMPTION OF ARTERIAL SMOOTH MUSCLE
CENTRE WELL
STEEL SUPPORT
ttt
\
ARTERIAL SEGMENT
FIGURE 5
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At left, the mounted artery (black area immediately
above arrows) is shown while relaxed, and at right
when it is maximally contracted by epinephrine (5 X
l(h7 g/ml). In each case the artery diameter was
measured with a travelling microscope at the three
points indicated, i.e., at centre and on each side of
centre at a distance equal to one-ninth the total secmental length. The average of these three readings
gave the average diameter. For this preparation the
percentage decrease in average diameter was calculated to be 12% of the relaxed average diameter.
Average diameter of this artery before mounting was
found to equal 2.5 mm. A qualitative estimate of its
degree of stretch could be expressed as the ratio:
annulus diameter (3.5 mm)/unmounted diameter (2.5
mm) or 1.4.
probable that either glucose or glycogen satisfies the major metabolic requirements of this
tissue while it is relaxed.
The increase in the degree of contraction
and of the Qo., with stimulation by epinephrine and norepinephrine was remarkably different in different experiments, ranging from
no significant changes to very large changes
(14% decrease in diameter and an 8()# increase
in Qd,,). We then realized that since the same
size annulus was used to mount arteries of
different diameters, they were submitted to
very different degrees of initial stretch. A
roughly quantitative estimate of this initial
stretch is given by the ratio of the annulus
diameter over the unmounted diameter of the
arterial segment (fig. 6).
The effect of initial stretch of arterial muscle on degree of contraction to pressor drugs
was shown for epinephrine by Sparks and
Bohr1* and for norepinephrine by Speden.1"
Our results indicate that a similar increase of
contraction for the same stimulus, and of Qo.,
Circulation Research, Vol. XVIII. January / % 6
85
to epinephrine and norepinephrine, occurs
with increased initial stretch of the muscle.
Epinephrine was used initially since it gave a
contraction that lasted longer, but was theoretically unsatisfactory owing to its possible general effects on the noncontractile portions of
the vascular smooth muscle cell; i.e., it may
stimulate the carbohydrate metabolism of
these tissues also. When norepinephrine was
used, contractions lasted for a shorter time, but
the increased rate of oxygen consumption was
comparable in magnitude to that produced
by epinephrine. This suggests that the changes
of oxygen consumption as measured by us
were due primarily to changes in metabolism
of the contractile portion of the muscle cell.
Since comparable concentrations of each drug
gave comparable amplitudes of response, in
terms of change both in percentage diameter
and in oxygen consumption, epinephrine was
finally preferred and used throughout subsequent experiments.
With an increased contractile response,
measured as a percentage decrease in outer
diameter, a corresponding, parallel, increase
in the resulting Qo., over the relaxed value was
also found. So, although the external work
done by the muscle contracting against the
restraint imposed by its tied ends is small,
the oxidative needs of its contractile structures
nevertheless increase significantly, up to twice
the resting oxygen consumption. As shown in
figure 6, although the Qo., during relaxation
does decrease slightly with increased initial
circumferential stretch of the segment, it is
not nearly sufficient to explain the large parallel increase observed in the ratio of contracted muscle Q()., to the relaxed muscle Q,,.,.
Hence, it is probable that the increase in the
excess O- consumption is due chiefly to the
increased degree of contraction by the muscle.
Also it is probable that the increased contraction is due to the increased sensitivity of
the stretched muscle to a constant concentration of added catecholomine.
More recently with a polarographic technique using arteries ranging in diameter from
2 to 4 mm we have found that with the same
initial tension (or stretch) and the same stimu-
86
KOSAN, BURTON
20
6
15-
10
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1.0
OS
10
1.4
1.8
MOUNTMG DIAMETER (3.5mm)
ARTERY UNMOUNTED DIAMETER
(DEGREE CIRCUMFERENTIAL STRETCH)
•O- -O- -O-
Oc2 RATIO
% DECREASE IN DIAMETER
RELATIVE CHANGE IN RELAXED QOi
FIGURE 6
When the circumferential stretch of the artery wall is increased, the relative decrease in
diameter and the relative increase in the oxygen consumption of the contracted artery change
in parallel manner. Same concentration of epinephrine (5 X 10~7 g/rnl) was used to stimulate
each preparation. With stretch, relatively little change is observed in the Qo of relaxed
(nonstimulated) artery. Solid triangles, dots, and squares represent corresponding average values
over the intervals indicated by their horizontal bars.
lation in each case there was no statistically
significant difference in the degree of contraction (actually, the active tension developed)
and in the Qo2 between the smallest and largest arteries studied. Presumably it is the degree of stretch rather than the arterial size itself that is the major cause of the increased
contraction and hence increased oxygen consumption observed wth our smaller arteries.
Bulbring,13 working with intestinal smooth
muscle and Evans15 with uterine smooth muscle, observed in most cases an increase in the
oxygen consumption of the muscle while it
was contracting isometrically, but a decrease
when the contraction was isotonic. This decrease during isotonic contraction was attributed to a decrease in the surface energy of
the muscle. This surface area, and perhaps the
surface energy, decrease in our experiments
also. There is evidently a difference in the
metabolic requirements of these smooth muscles (intestinal and uterine vs. vascular smooth
muscle) when contracted. As shown in figure
6, the oxygen consumption of the relaxed
muscle decreased somewhat with increased
circumferential stretch. Bulbring, using intestinal muscle, observed the opposite.13 Experiments prior to these, and some since, inCirculation Research, Vol. XV111, January 1966
OXYGEN CONSUMPTION OF ARTERIAL SMOOTH MUSCLE
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dicate that the Q0o of the unstretched relaxed
artery does not change significantly from the
largest to the smallest arteries that we have
studied. Howard et al.20 have recently shown
that with arterioles, the relaxed muscle Qo.,
generally increases with decreasing size. With
our larger arteries this was not apparent.
It has been thought possible that in vascular
smooth muscle as in other types of smooth
muscle, especially molluscan smooth muscle,
a catch mechanism may permit a prolonged
contraction to take place without a corresponding increase in the energy turnover of the
muscle. Our results indicate that it is doubtful
that such a mechanism operates in arterial
smooth muscle in arteries of the size we used
(though of course the mechanism in small vessels such as arterioles might be different).
It is noteworthy that with this multi-unit
arterial smooth muscle the initial stretch did
not increase the resting oxygen consumption of
the arterial wall, so no support is given by
these results to the suggestion that stretch of
vascular smooth muscle is, per se, a stimulus
to contraction (myogenic theory). However,
stretching this muscle greatly increases its
response, in degree of contraction and in Oj
.consumption, to the stimulus of pressor drugs.
If, in normal function, there is always some
vasoconstrictor arterial tone, then stretching
the wall by transmural arterial pressure will
increase the tone of its vascular smooth muscle. On the other hand, in completely relaxed
vascular smooth muscle, as in dilated arteries,
a rise in blood pressure would not produce
any increase in tone and consequent constriction. On this basis, some of the apparent contradictions in the literature as to the existence
of the myogenic reflex may be brought into
agreement.
Summary
The mean oxygen consumption of relaxed
isolated vascular smooth muscle segments was
found to equal 0.61 ±0.94 SEM /iliter/mg wet
wt/hr in a medium of buffered Ringer-glucose,
and 0.65 ± 0.05 SEM /iliter/mg wet wt/hr in a
solution of dog plasma. The resting muscle RQ
was found to equal 0.99 ± 0.01 SEM in buffered
Ringer-glucose solution. When stimulated by
Circulation Research, Vol. XVIII, January 1966
87
addition of epinephrine the muscle segment
contracted on the average by 9% of its initial
diameter with a corresponding increase of its
oxygen consumption by an average of 30% over
its relaxed value. It was noticed that with increased initial circumferential stretch of the
muscle segment, the amplitude of contraction
was much greater when a given amount of
catecholamine was added. This increase of
sensitivity to catecholamine produced by initial
stretch, was accompanied by a parallel increase of oxygen consumption by the contracted muscle. A qualitative correlation between
an estimated degree of contraction of arterial
muscle and its oxygen consumption was demonstrated. More quantitative correlation will
have to depend upon better methods of measuring both the tension developed and the degree of initial stretch.
Appendix
SAMPLE CALCULATION:
From segment I, (with CO 2 absorber) we know
that for oxygen consumption, X Qo :
X
O 2 = h O 2 X K 02 , when:
h 0 o = change in manometer reading per unit time
(e.g., in one hour)
KOl) = flask constant for oxygen in mm2
" =0.497 mm/mg wet wt/hr X 1.18 mm2
= 0.59 juliter 0 2 /mg wet wt/hr
From segment II, (without CO, absorber) we know
the net change in the manometer reading h n , to be
equal to h^^ — h c o o
n = h O 2 "" h C(V o r hco 2 — h O 2 — hn
But h n was found in this experiment to equal 0.366
mm/mg wet wt/hr
and h Oo
= 0.497 mm/mg wet wt/hr, assuming it
to be the same as segment I
= 0.497-0.366
"OOo
= 0.131 mm/mg wet wt/hr
or h
X COo
where KCOo =4.49 mm2 (corrected for buffer retention)
= 0.131 mm/mg wet wt/hr X 4.49 mm2
X
co2
= 0.59 filter CO 2 /mg wet wt/hr
In this particular case:
88
KOSAN, BURTON
Respiration of rat thoracic aorta. J. Biol.
Chem. 179: 103, 1949.
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LUNDHOLM,
L.,
MOHME-LUNDHOLM,
E.:
KIRK, J. E., EFFERSOE,
P. G., CHIANG, S. P.:
The rate of respiration and glycolysis by human and dog aortic tissue. J. Geront. 9: 10,
1954.
4.
HENDERSON, A. E., AND MACDOUCALL, J. D. B.:
The respiration of arterial tissue. Biochem. J.
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5.
MAIER, N., AND HAIMOVICI, H.: Metabolism of
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Circulation Research, Vol. XVlll,
January 1966
Oxygen Consumption of Arterial Smooth Muscle as a Function of Active Tone and Passive
Stretch
R. L. Kosan and Alan C. Burton
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Circ Res. 1966;18:79-88
doi: 10.1161/01.RES.18.1.79
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