Effects of Bladder Distention on Pulmonary Vascular Bed
By ALBERTO AGREST, M.D., AND AQUILES J. KONCORONI, M.D.
jection was performed rhythmically, every 2 seconds, timed with a metronome set at 60 beats/min.
The amount of dye introduced was measured
by weighing the syringe before and after the
injection. The dead space of the catheter and
manifold, through which the injection was performed, was measured by tho weight difference of
the system, when dry and when filled with distilled water. The dye remaining in the catheter
was washed out by aspirating 10 ml. of blood
immediately after the injection. Blood for hematocrit determination and for the plasma blank of the
dilution curves was sampled from the artery prior
to the injection.
Tubes were spun in a centrifuge at 3,000 r.p.m.
for 30 minutes. Dye concentrations in plasma
were read in a Beckman Model DU spectrophotometer at 6.250 A0 wavelength. The hematocrit was
determined by centrifuging the heparinized blood
in Wintrobe tubes for 30 minutes at 3,000 r.p.ni.
Dye concentrations were plotted in semilogarithmic
paper, with extrapolation of the straight descending line previous to recirculation.
The cardiac output was computed from the dye
dilution curve according to the method of Hamilton, Moore, Kinsman and Spurling.4 Mean circulation time was computed according to the formula
of Etsten and Li.5 Central blood volume was
computed by the Stewart principle.0' 7
Total blood volume was measured with Evans
blue dye, taking blood samples at the tenth and
twentieth minute after the injection, but assuming
the tenth minute samples as the value of complete
homogenization in these patients, according to
Gregersen's method.8
Cardiac output by direct Fick method was
detei'mined by collecting expired gas in a Douglas
bag during 5 minutes and sampling blood from
the pulmonary and femoral arteries dimng the
third minute. Blood gases were determined in
duplicates according to the teehnic of Van Slykc
and jSTeill, blood pH in a glass electrode with a
Beckman G potentiometer. Expired air was measured in a calibrated Tissot spirometer and duplicate analysis for O2 and C0 2 were carried out
in a Scholander gas analyzer.
Femoral and pulmonary artery pressure were
measured with a Statham strain-gage transducer,
the zero point of reference being 10 cm. above
the level of the table. A Sanborn Twin-Viso was
used as recording system. Average systolic and
B
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LADDER distention is known to produce
vascular and other autonomic reactions,
which are much more evident in paraplegics
than in normals and is more important the
higher the level of spiual cord transection.
These autonomic reactions include increased
arterial pressure caused by systemic vasoconstriction, headaches, flushing of the face,
bradycardia and sweating.1 We planned to investigate if the pulmonary vascular bed was
included in this reaction and so demonstrate
an example of nervous control of pulmonary
vessels, a long debated subject.2 Our results
seem to offer a good argument in favor of this
nervous control and demonstrate that the pulmonary vascular bed participates in the general effects of bladder distention.
Methods
Hemodynamic studies were performed in 2 paraplegic patients. One of them (case 1), a 22-yearold male, had a spinal cord transection at C6
level, caused by a gunshot wound 2 years prior
to this study. Case 2, a 32-year-old female, had
a chronic transverse myelitis of unknown origin
at C5 level. Both patients could breathe spontaneously, using diaphragmatic muscles and both
of them had no control of their bladder functions.
Venous catheterization was performed with a
single lumen cardiac catheter, guided under fluoroscopy and left in the pulmonary artery trunk
just beyond the pulmonic valve. An indwelling
Cournand needle was placed in the femoral artery.
Cardiac output was determined simultaneously,
as described below according to direct Fiek and
Stewart-Hamilton principles.3
Cardiac output determination by the dye dilution technic followed the injection of a 0.5 per cent
solution of Evans blue dye into the pulmonary
main artery and collection of samples from the
femoral artery. Blood was collected into heparinized test tubes through the Cournand needle and
a plastic tube (22 cm. long and 2 mm. bore).
" Sampling of blood, starting 5 seconds after the in—
Prom tho Centro de Rohabilitacion Respiratoria,
Ministerio -de Asistoncia Social y Salud Publica de la
Naci6n, Patagones 849, Buenos Aires, Argentina.
Received for publication October 5, 1959.
Circulation Research, Volume VIII, May 1960
501
AGREST, RONCORONI
502
Table 1
Respiratory Data
£
c
1
21
2
38
1.63
M
0
25
3.56
3.12
2.41
1.91
13
15
446
340
143 115
134 98
137
110
.835
.890
96.5
48.9
7.43
95.3
50.9
7.38
0
30
3.89
4.05
1.72
2.09
22
20
279
321
155
84
.826
.785
45.3
7.35
92
102
118
94.2
152
96.0
44.7
7.39
VB ml.
Sex
VT ml.
B.S.
O
Vesical
pressure
cm. H2O
Case Age
_£
a
1
S
6
6
0
a
O
X
a
PS
6*
41
44
42
38
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All pulmonary volumes are B.T.P.S.
V = expired volume; VA = alveolar ventilation; f = respiratory rate; VX = tidal volume;
VD = dead space volume (includes instrumental dead space = 72 ml.); V CO2 = COa production; Vos = 02 consumption; E = respiratory quotient; 8aOs = oxygen arterial saturation;
C:iCO2 = arterial CO? content; PaCO» = arterial PCOa.
diastolic pressures were measured over at least
2 respiratory cycles, while mean pressures were
obtained by planirnetrie integration.
Vesical pressure was measured directly with a
water manometer, zero level being set also 10 cm.
above the level of the table.
With the patient supine, the catheter placed
in the pulmonary artery, a Foley catheter in the
bladder and breathing through a low resistance
respiratory valve, a large 3-way stopcock allowed
us to collect expired air into a Douglas bag. A
manifold connected to the cardiac catheter permitted us either to preserve the patency of the
catheter with a 5 per cent glucose drip, to connect
the strain-gage or to inject the dye and draw the
mixed venous sample. The bladder, emptied just
prior to the procedure, was connected either to a
collecting bottle, to a source of saline solution or
to a water manometer through a glass 3-way
stopcock. Once expired air collection was started,
arterial blood was sampled for hematoerit and
blank of the dye dilution curve. Immediately
thereafter, a quick injection of the dye solution
was made through the manifold and catheter into
the pulmonary artery, discontinuing the pulmonary
artery pressure recording started at the same
time as the gas collection. When the injection
was finished, pulmonary artery pressure was again
recorded, while arterial blood was sampled every
2 seconds up to the thirty-seventh second. Immediately thereafter, 10 ml. of blood were drawn
from the pulmonary artery in order to wash out
the dead space of the catheter, and blood for gas
analysis was then withdrawn simultaneously from
pulmonary and femoral artery during the third
minute. At the end of arterial blood sampling,
the Cournand needle was connected to the Statham
transducer and femoral artery pressure was re-
corded. Ten and 20 minutes after the injection of
the dye, blood was sampled from the artery for
blood volume determination. While pulmonary
artery pressure was being recorded, the bladder
was filled by step wise injection of 50 ml. of saline
solution and alternatively connected to the water
manometer. After introducing 200 ml., the vesical
pressure was sufficiently increased, although it
did not stay at 1 level for long, probably due to
changes in vesical tonus. The whole procedure
previously described was now repeated. Pulmonary
and total peripheral resistances were calculated
by the formulas:
Pulm. art. resist, in dynes, sec. cmr6 =
mean pulm. art. pressure mm. Hg X 1,332.
Cardiac output ml./sec.
Total peripheral resistance =
mean femoral artery pressure mm. Hg X 1,332.
Cardiac output ml./sec.
Results
Table 1 shows the respiratory data of both
patients with bladder empty and rilled to a
pressure of more than 25 cm. of water. Ventilation was within normal limits and changes
with increased vesical pressure were small.
Table 2 shows the hemodynamic data.
Cardiac output, as determined by the dye
dilution method, was normal and no significant
change was observed on increasing vesical
pressure. A small fall of cardiac index was
demonstrated by the Fick principle. Mean
circulation time diminished slightly in case 1
and did not change in case 2. '' Central blood
Circulation Research, Volume VIII, May I960
503
PULMONARY CIRCULATION AND BLADDER DISTENTION
Table 2
Hemodynamic Data
Vesical
pressure
Case cm. HsO
0
>25
Qs
ml./
C.I.F C .I.H DA-V02 M.C.T. Qc
vol. % sec. L./m.= Kg.
L./min.
3.31 2.29 4.14 18.01 .688 75.8
2.59 2.16 4.23 15.20 .547 83.0
Hct.
43.,5
43..0
H.R.
mm.
75
66
P.A .P. mm. Hg
D.
M.
mm.
12.1
20.4
2.6
6
8.5
12.6
F.P. mmi. Hg
M.
M. D.
78
116
P.R. P.T.R.
dynes
sec. cm."0
182
286
1.410
2.230
+48 +57
+58
66
61
88. 5 98
1
Change
0
30
Change
%
-21
-6
+2
-12
-20
+9
0
2.26
2.44
3.08
3.33
4.49
4.67
14.0
14.35
.720
.797
66.9
70.9
44.0
44.0
+7
+8
+3
+2 +10 +6
0
+48
-12
93
81
-13
13.1
20.4
4.4
6.8
8
14
+ 75
97
112
65
78
81
95
131
216
1.329
1.445
+17 +65 + 9
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C.I.IT = cardiac index (Pick) ; C.I.H — cardiac index (Hamilton); DA-VOS = arterio venous
O2 difference; M.C.T. = mean circulation time; Qc = " c e n t r a l " blood volume; Qs = blood
volume; H.R. =: heart rate; P.A.P. = pulmonary artery pressure; P.P. = femoral artery
pressure; P.R. = total pulmonary resistance; P.T.R. = peripheral total resistance.
volume'' showed small and inconsistent variation. Changes in blood volume were also very
slight and the hematoerit remained the same.
Pulmonary artery pressure increased in
both cases, 48 per cent in the first (fig. 1) and
75 per cent in the second (fig. 2). Pulmonary
resistance, computed from dye dilution output, increased 57 per cent in the former and
65 per cent in the latter. These are rather
striking changes when compared with the
smaller increase in femoral pressure and peripheral total resistance, especially in case 2.
Figure 3 shows the pulmonary artery pressure recording at different vesical pressure
levels. Once pulmonary artery pressure has
risen with bladder distention, it remains high,
even when vesical pressure decreases from 65
to 10 cm. of water.
Discussion
Effects of bladder distention on autonomic
mechanisms in paraplegic patients were reviewed and studied byGuttmann and Whitteridge1 in 1947, and by Hutch9 in 1955.
These effects have been classified as: (a) mass
involuntary, peripheral muscle spasm ; (b) hyperactive reflex of sympathetic nervous system
manifested by rise in arterial pressure, pilomotor and sudomotor responses; and (e) mass
parasympathetic reaction observed as bladder
spasm.
Circulation Research, Volume VIII, May 1960
The effects that were secondary to the increased arterial pressure were as follows: (1)
bradycai'dia due to carotid sinus and aortic
arch stimulation; (2) headaches, due to passive cerebral vasodilation with increased cerebral blood flow; and (3) patchy vasodilation
of the skin of the face and neck and of the
nasal passages due to reflex or passive vasodilation. Guttmann also observed engorgement
of the veins of the neck, marked dilation of
the heart, tightness of the chest and shallow
breathing, a situation resembling incipient
heart failure.
Our subjects show increase in peripheral
and pulmonary resistance. Since increased
pulmonary artery pressure in this condition
has not been described before, we shall discuss
this point. Pulmonary artery pressure is increased when intrathoracie pressure rises during a sustained expiratory effort. Bladder distention may cause mass voluntary muscle
spasm and increase intrathoracie pressure, but
this is only a very transient effect that did
not appear during our pressure recording.
Normal respiratory cycles can be seen in the
records (figs. 1 and 2) and excludes a Valsalva
type of effect. Therefore one can accept increased pulmonary artery pressure as a circulatory effect.
Pulmonary arterial pressure may increase
because of increase in cardiac output or in
AGREST, RONCORONI
504
VESICAL PRESSURE 0
VtSICK PRCSSUK • 0
VESICAL PRESSURE>2f<_K
v i s i c u MESWK>U_iU>
f«mer»l Arttry fVttSur*
: l '
Pulmontrj A r t i r j
PrgJSure
Figure 1
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Pulmonary and femoral arterial pressure effects
of increasing vesical pressure. Case 1.
Pulmtntry Artarj Prt»»ur«
Figure 2
Pulmonary and femoral arterial pressure
of vesical pressure. Case 2.
effects
V«s.c«l
Hcm.H.0
|
Figure 3
Pulmonary arterial pressure effects of increasing vesical pressure.
resistance. Cardiac output rise was shown not
to occur and may be excluded.
A rise of resistance in this condition may
occur as a consequence of left heart failure,
pulmonary vein constriction or constriction
of pulmonary arterioles. This point has not
been elucidated in our experiments because
"capillary" pulmonary pressure was not recorded, but the rather small increase in systemic arterial pressure and lack of rise in central blood volume speak against left heart
failure.
Constriction of the venous side of the pulmonary vascular bed cannot be excluded, although lack of significant ventilatory changes
would not favor this interpretation.
Pulmonary arteriolar vasoconstriction is
left as the more plausible explanation. Is this
increase in resistance mediated through a
nervous or a humoral stimulus? Although a
reflex phenomenon seems more probable, the
fact that pulmonary artery pressure remains
47cm.H»0.
Case 1.
high, even when the vesical pressure has fallen to zero and returns to previous levels after
about 10 minutes, calls for the possibility of a
humoral mediator. Bpinephrine, norepinephriue and histamine may be excluded, the
first because cardiac output did not increase,
the second because pulmonary resistance increased more than the peripheral resistance,
and the third because the systemic pressure
rose. Sei'otonin is still left as a possible humoral factor in this reaction that would explain the rise in pulmonary artery pressure.10
The other hemodynamic effects of this substance have numerous circulatory actions, so
that any combination may be expected.11
Pathogenesis of the rise in pulmonary artery
pressure with bladder distention, in spinal
cord section, remains an open question.
Summary
Hemodynamic data during bladder distention in 2 patients with cervical cord transacCirculation Research,
Volume VIII, May 1960
PULMONARY CIRCULATION AND BLADDER DISTENTION
tion are presented. Rise in pulmonary artery
pressure and pulmonary resistance is shown
to occur when vesical pi'essure is increased.
Summario in Interlingua
Es presentate datos hemodynamic obtonite durante
distension del vosica in 2 patientes con transsection
del cordon cervical. Es monstrate que augmentos del
tension pulmono-arterial e del resistentia pulmonar
orcurre quando lo pression del vosica es auginentate.
References
1. GUTTMANN, L., AND WHITTERIDGE, D.: Effects of
bladder distension on autonomic mechanisms
after spinal cord injuries. Brain 70: 361, 1947.
2. COURNAND, A.: Historical development
of
the
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concepts of pulmonary circulation. In Pulmonary Circulation, W. E. Adams and Ilza Veith.,
Ed. New York, Grune and Stratton, 1959.
3. HAMILTON, W. F., and others: Comparison of the
Fick and dye injection methods of measuring
cardiac output in man. Am. J. Physiol. 153:
309, 1948.
4. — , MOORE, J. W., KINSMAN, J. M., AND SPURLING, E. G.: Studies on the circulation. IV.
Further analysis of the injection method and
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5. ETSTEN,
B.,
AND L I , T.
H.:
Hemodynamic
Circulation Research, Volume VIII, May 1)00
505
changes during thiopental anesthesia in humans: Cardiac output, stroke volume, total
peripheral resistance and intrathoracic blood
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6. STEWART, G. N.: Pulmonary circulation time, the
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7. HAMILTON, W. F., MOORE, J. W., KINSMAN, J. M.,
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the mean velocity of blood flow through the
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9. HUTCH, J. A.: Study of the hyperactive autonomic reflex initiated by bladder distention in
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10. COMROE, J. H., VAN LINDEN, B. STROUD, B. C,
AND EONCORONI, A.: Reflex and direct cartliopulmonary effects of 5-OH-Tryptamine (serotonine). Am. J. Physiol. 173: 379, 3953.
11. PAGE, I. H.: Serotonine (5 Hydroxitryptamine) ;
the last four years.
1958.
Physiol. Eev. 38: 277,
Effects of Bladder Distention on Pulmonary Vascular Bed
ALBERTO AGREST and AQUILES J. RONCORONI
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Circ Res. 1960;8:501-505
doi: 10.1161/01.RES.8.3.501
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