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From Biology of the Vascular Wall, INSERM Units 141 (O.L., E.M., P.P.,
B.I.L.) and 337 (M.E.S.), IFR Circulation, Hôpital Lariboisière,
Paris, France.
Correspondence to Bernard I. Levy, INSERM Unit 141, 41 Blvd de la Chapelle, 75475, Paris, France. E-mail levy{at}infobiogen.fr
Abstract
Abstract—Several recent
results obtained in hypertensive animals and subjects under in vivo
isobaric conditions do not confirm the classic view of stiffer arteries
in hypertensive subjects. We compared the mechanical behavior of in
situ isolated common carotid arteries from normotensive Wistar-Kyoto
rats (WKY) and age-matched spontaneously hypertensive rats (SHR) under
both static and dynamic conditions for transmural pressure ranging from
50 to 200 mm Hg. The static pressure (P)–diameter (D)
relationship was shifted to higher values of diameters in the SHR
mainly because of a larger unstressed carotid diameter (Do)
in hypertensive rats. The carotid mechanical strain, calculated as
(D-Do)/Do, was significantly reduced in SHR at
pressure levels between 100 and 200 mm Hg. The static carotid
compliance and distensibility were markedly smaller in SHR than in WKY
carotid arteries, indicating a stiffer wall in hypertensive animals. In
contrast, carotid compliance and distensibility were similar under
dynamic conditions close to the in vivo pulse pressure (frequency, 300
bpm; peak amplitude of the oscillatory pressure, 20 to 25 mm Hg).
However, marked differences in dynamic compliance- and
distensibility-strain relationships in SHR and WKY are evidence of
clearly different arterial wall material properties in both
strains. We therefore conclude that larger lumen carotid arteries in
hypertensive rats could compensate for a stiffer arterial
wall, resulting in similar dynamic compliance and distensibility in
normotensive and hypertensive rats.
There is
general agreement that arterial hypertension, aging,
diabetes, and atherosclerosis are associated with
marked changes in structure and mechanical properties of large
arteries.1
Because of the nonlinear pressure-diameter relationship of large
arteries, it is difficult to compare the mechanical properties of the
large arterial wall in patients or animals with different
arterial blood pressure. Furthermore, most of the
experiments to assess the mechanical properties of the
arterial wall are performed under static conditions, ie,
with the pressure being varied by successive
steps.2 3 However, under in vivo conditions with
pulsatile pressure generated by the cardiac pump, the large
arterial wall must be considered in terms of dynamic
behavior, ie, taking into account the viscous, frequency-dependent
properties of the vascular wall.
New ultrasonic technologies have been developed that allow the
precise measurement of both in vitro and in vivo instantaneous
arterial diameter.4 The application
of these ultrasonic techniques to the calculation of mechanical
properties of large arteries in human and experimental hypertension has
led to conflicting results. In contrast to the classically reported
stiffer arterial wall in hypertensives, similar or even
increased arterial compliance and distensibility were
calculated in hypertensive subjects and
animals.5 6 However, because of in vivo
measurements in the operating arterial pressure range, it
was impossible to compare the dynamic mechanical properties of the
arterial wall in hypertensives and normotensives under
isobaric conditions without an unverified hypothesis and theoretical
models of the mechanical behavior of the arterial wall. In
fact, to compare the arterial wall properties in vivo under
isobaric conditions in normotensives and hypertensives, one must use
calculations performed from pressure-diameter values recorded
during the systole in the former and during the late
diastole in the latter, ie, under markedly different
dynamic conditions. It is also possible to modify the operating
pressure in 1 group to reduce the arterial pressure in
hypertensives and/or to increase it in normotensives, and therefore to
compare wall properties in normotensive and hypertensive animals at
comparable blood pressures in vivo.7 However, the
calculated parameters do not represent their actual
operating values; furthermore, a direct effect of the drugs used to
modify the arterial pressure on arterial smooth
muscle tone and mechanical properties cannot be excluded.
Therefore, the purpose of the present study was to (1) describe an
experimental setup that would allow us to simultaneously
evaluate in situ the static and dynamic properties of the CCA in
normotensive WKY and SHR and (2) differentiate from the alterations of
the mechanical arterial properties in SHR those that are
related to the static properties (pressure domain) and those related to
the dynamic properties (frequency domain) of the vessels.
Methods
Experimental Setup and Artery Preparation
Eight 12-week-old normotensive control rats (WKY) and 8 age-matched SHR
were anesthetized with sodium pentobarbital (50 mg/kg IP) and
kept at constant body temperature (38°C) with a thermostatic
operating table (Harvard Apparatus). After
anesthesia, the trachea was cannulated and connected to a
rodent respirator (model 680, Harvard Apparatus). The left
CCA was then exposed, and its upper end was catheterized with a
10-cm-long noncompliant tube (Teflon, 0.9 mm ID) filled with
Tyrode's solution containing albumin (4%). A noncompliant
tube, as short as possible, was used to minimally affect the mechanical
properties of the carotid segment. The tube used was at least 10 000
times stiffer than the carotid segment. The presence of protein in
flushing and incubating solutions preserved the
endothelium and maintained a
physiological osmotic pressure gradient across the
vessel wall. The root of the left carotid was dissected, and a 2F
microtip pressure transducer (Millar) was inserted into the CCA. The
upper end of the CCA was connected to a pressure chamber with
adjustable steady pressure (windkessel system); pressure sinus waves
were superimposed in the isolated segment of carotid artery by means of
a vibrator (LSD, model 200) with an amplifier (LSD, model PA25E)
connected to the upper end of the artery (frequency, 300 bpm; peak
amplitude of the oscillatory pressure, 20 to 25 mm Hg).
For the arterial diameter measurement, a high-precision
ultrasonic echo-tracking device was used (Asulab). The probe consisted
of a 10-MHz strongly focused piezoelectric transducer (6 mm
diameter, 11 mm focal length) operated in the pulse-echo mode. The
-10 dB beam width is 0.3 mm at the focal point, and the depth of
field at -10 dB is 5 mm. A stereotaxic arm permitted
motion of the transducer in x, y, and
z coordinates with micrometric steps to place the probe
perpendicularly to the arterial axis in its largest
cross-sectional dimension. The transducer was positioned so that its
focal zone was located in the center of the artery; thus, the
back-scattered echoes from both the anterior and posterior walls could
be easily visualized. A typical RF signal is then displayed on a
computer monitor interfaced to the transducer system.
Arterial diameter was measured when a clear
"double-peak" RF ultrasound signal of the anterior and the
posterior wall was obtained. These signals are only visible as the
ultrasound beam crosses the axis of the vessel and are characterized
first by a high-amplitude signal followed by a relatively silent
acoustic period and then a second high-amplitude signal.
The sample rate of the system is 5000 Hz, and its resolution is close
to 1 µm. To enlarge the acquisition capacity, each consecutive
16 points were averaged into a single value, meaning that the actual
sample rate is 312.5 Hz. The difference between 2 successive
measurements was <2 µm.8
Protocol and Data Acquisition
From the instantaneous pressure and diameter signals, the mean diameter
and mean pressure were calculated. The power spectrum analysis
of the signals was done using the standard signal processing toolbox of
MATLAB and the Welch method of power spectrum
estimation.9 The sequence of N points was divided
into K sections of M points each (M must be a power of 2). Using an
M-point fast Fourier transform, successive sections were Hanning
windowed, analyzed, and accumulated. After processing of the
spectral analysis of the signal, the amplitudes of the first
harmonic of pressure (dP) and diameter (dD) were obtained.
Calculation of Mechanical Properties
For static variables, unstressed diameter
(Do) and volume (Vo) were
considered to be diameter and volume values at 50 mm Hg
transmural pressure. Strain was calculated as
(D-Do)/Do (dimensionless
parameter). The static compliance per unit length was
defined for each pressure step as C=
For dynamic variables, measurements were performed at each step of
transmural pressure P, corresponding to a static diameter D. At each
value of P, a sinus pressure wave signal dP produced changes in
diameter dD and corresponding changes in cross-sectional area dS,
assuming a cylindrical model of the artery. In this system, dynamic
compliance and distensibility, expressed per unit length of the artery,
were respectively calculated as dS/dP and
(dS/So)/dP, with So
(unstressed lumen
area)=
Statistical Analysis
Results
Under Static Conditions
Figure 1
Under Dynamic Conditions
Figure 3
Figures 4
Discussion
The structural changes of the arterial wall
observed in hypertensive patients and animals may reflect either a
primary defect or a consequence of elevated blood pressure. Increased
vascular wall thickness, a constant feature reported in sustained
hypertension, is thought to be a key determinant of the mechanical
behavior of large arteries. Several physical parameters
have been used to assess the influence of hypertension on the
arterial mechanical properties. Pulse wave
velocity,10 analysis of the exponential
diastolic pressure wave decay,11 and
analysis of the pressure-diameter
relationship12 are among the approaches used to
characterize the mechanical properties of the arterial wall
associated with hypertension. Compliance, which can be defined as the
blood volume stored or released for a given arterial pulse
pressure, decreases when mean blood pressure increases. Because the
pressure-volume relation is clearly nonlinear,13
compliance changes dramatically with variations in blood pressure.
Therefore, pressure has to be accounted for as a variable. This is
not possible in vivo when mechanical properties of arteries have to be
compared under normal and hypertensive conditions.
In the present series of experiments, the in situ isolated
segment of rat CCA was studied under controlled values of transmural
pressure (50 to 200 mm Hg), allowing us to correctly compare the
calculated mechanical parameters in normotensive and
hypertensive rats. In terms of functional changes in pathological
conditions, information from the carotid bulb would be more relevant;
however, the ultrasonic system used in this and in most experimental
and clinical studies does not allow reliable recording of
diameters in noncylindrical vessels.
Furthermore, in most previous studies, the mechanical properties
of the arterial wall have been considered under static
conditions. Basically, when blood pressure increases, the lumen
arterial diameter increases and energy is stored in the
vascular wall. Purely elastic materials allow the whole stored energy
to be restored during diastole. However, the
arterial wall exhibits viscoelastic behavior, and a part of
the stored energy is dissipated within the arterial wall
because of viscous properties of the wall.14 15
In a recent extensive in vivo and in vitro study, Boutouyrie et
al16 showed that the viscous loss of energy
appeared to be small at the cross-sectional level but cannot be
neglected if it is integrated along the arterial tree. We
used a pulse pressure value of 25 mm Hg to mimic the in vivo
pressure. The pulse pressure values are different in normotensive and
hypertensive animals, and our experimental conditions were as close as
possible to the in vivo conditions but did not perfectly fit to the in
vivo models.
One of the main findings of the present work is that the mechanical
properties of the carotid arterial wall are markedly
different under steady (static) and pulsatile conditions, indicating
stiffer arterial wall for pulsatile pressure. Under static
conditions, carotid compliance and distensibility were markedly reduced
in the SHR, in agreement with previously reported results under similar
conditions.17 18 In contrast, under dynamic
conditions, carotid compliance and distensibility appeared to be very
similar in normotensive and hypertensive rats. This latter result can
be compared with those obtained by several
investigators5 6 under in vivo pulsatile
conditions. Our present study confirms most previously reported
results; however, its major interest lies in the comparison of static
and dynamic properties of the carotid wall in the same animals.
Furthermore, from similar values of dynamic arterial
compliance and distensibility in normotensive and hypertensive animals
and subjects, it is generally inferred that the arterial
tissue has similar mechanical properties in both populations
(normotensive or hypertensive). However, comparison of the mechanical
properties of the arterial wall submitted to different
transmural pressures must be made with caution. When expressed as
dynamic compliance or distensibility versus pressure values, there were
no differences in behavior between carotid arteries from normotensive
and hypertensive rats. Conversely, when expressed versus the carotid
strain, representing the relative stretching of the vessel,
the behavior of the carotid wall was markedly different in normotensive
and hypertensive rats. This result is due mainly to the larger
unstressed diameter of carotid arteries from hypertensive rats.
However, we can exclude that the mechanical properties of the
arterial tissue is similar in normotensive and hypertensive
animals. We therefore suggest that larger lumen carotid arteries in
hypertensive compared with normotensive rats could compensate for
stiffer arterial wall, resulting in similar in vivo
(dynamic) compliance and distensibility in normotensive and
hypertensive rats.
Selected Abbreviations and Acronyms
Received January 24, 1998;
first decision February 22, 1998;
accepted April 9, 1998.
References
1.
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Noninvasive assessment of the age-related changes in stiffness of major
branches of the human arteries. Cardiovasc Res.. 1987;21:678–687.[Medline]
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Hallock P, Benson IC. Studies on the elastic properties
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Learoyd BM, Taylor MG. Alterations with age in the
viscoelastic properties of human arterial walls. Circ
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Boutouyrie P, Bezie Y, Lacolley P, Challande P,
Chamiot-Clerc P, Benetos A, de la Faverie JF, Safar M, Laurent S. In
vivo/in vitro comparison of rat abdominal aorta wall viscosity:
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Thromb Vasc Biol.. 1997;17:1346–1355.
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Safar ME, Camilleri JP. Effects of chronic inhibition of converting
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Levy BI, Benessiano J, Poitevin P, Safar ME.
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© 1998 American Heart Association, Inc.
Third Workshop on Structure and Function of Large
Arteries: Part II
Static and Dynamic Mechanical Properties of the Carotid Artery From Normotensive and Hypertensive Rats
Key Words: carotid arteries • stiffness • viscosity • blood pressure
The experimental setup allowed us to maintain the CCA at
constant levels of mean pressure throughout the study and to
superimpose to the mean pressure a sinusoidal pressure wave of
adjustable frequency and amplitude.
In normotensive WKY and SHR, the in situ isolated CCA was
exposed to stepwise pressure increases of 25 mm Hg each step,
from 50 mm Hg to 200 mm Hg. Pressure-diameter relationships
were determined under static and then under dynamic conditions (5
minutes per step plus 5 minutes for recovery at each step). To obtain
oscillatory pressure, a sinusoidal wave of 5-Hz frequency with a
peak-to-peak amplitude of 20 to 25 mm Hg was superimposed over
each mean pressure. The ultrasound probe was positioned perpendicularly
over the artery with an ultrasound gel to avoid direct contact. After
each change in pressure, the new conditions were maintained for 4
minutes to let the tissue reach its steady state. At each pressure
level, the pressure and diameter signals were continuously measured for
4 seconds.
Using the measured static values of the "in situ" carotid
lumen diameter (D, µm) from 50 to 200 mm Hg and the
measured dynamic values dD (µm) and dP superimposed at each pressure
(P) step, several variables were calculated. 
V/P (µL/mm Hg), where V
is the change in volume V (with V=
D2/4)
induced by a transmural pressure variation of P (25 mm Hg) in
an artery segment of 1 mm in length. The static distensibility was
defined for each step of transmural pressure as
Dist=C/Vo and expressed per unit length
(10-3 mm Hg-1). Do2/4.
Results are expressed as mean±SEM. Two-way ANOVA was used to
test for significant differences between groups. Bonferroni's test was
used to detect differences for determined levels of pressure with
correction for multiple comparisons. A level of P<0.05 was
considered significant.
The Table
reports the
diameter-pressure and strain-pressure static values in WKY and SHR;
static diameters were significantly higher in SHR than in WKY at any
given value of transmural pressure (P<0.001). For
transmural pressure values >75 mm Hg, strain was significantly
higher in WKY than in SHR (P<0.001).
View this table:
[in a new window]
Table 1. Lumen Diameter and Wall Strain of Common Carotid Artery
Submitted to Increasing Levels of Static Transmural Pressure shows the curve relating
transmural pressure to static compliance and distensibility of the
isolated segment of the CCA. In both WKY and SHR, static compliance
(Figure 1A) decreased when transmural pressure increased. Except for
the extremities of the curves (50 to 75 and 175 to 200 mm Hg),
static compliance was significantly lower (P<0.02) in SHR
than in WKY. Figure 1B illustrates similar findings for the
distensibility-pressure curves; static carotid distensibility was
significantly lower (P<0.001) in SHR than in WKY for
pressures ranging from 75 to 175 mm Hg.
View larger version (16K):
[in a new window]
Figure 1. Static conditions: compliance (A) and
distensibility (B) of the in situ isolated CCA vs transmural pressure.
indicates WKY; 
, SHR. Values are mean±SEM. Differences between
WKY and SHR: *P<0.02 **P<0.001.
Figure 2 shows the experimental
relationships between transmural pressure and carotid lumen diameter in
both normotensive and hypertensive rats. Curvilinear curves (thin
lines) were obtained by joining the mean values of oscillatory
pressures and diameters at each pressure step. The phasic changes in
diameter (dD) induced by sinus pressure waves (dP) were superimposed
(bold lines) at each pressure steps. Two major points resulted from
these data: (1) there was no difference between the static
pressure-diameter carotid relationship and that obtained under dynamic
conditions by using the mean pressure and diameter calculated from
their phasic values; and (2) at each transmural pressure step, the
slope of the pressure-diameter static relationship was steeper under
static than under dynamic conditions, indicating stiffer arteries under
static pressure conditions.
View larger version (15K):
[in a new window]
Figure 2. Static (thin lines) and dynamic (bold lines) lumen
diameter-pressure relationships of the in situ isolated CCA vs
transmural pressure. indicates WKY; , SHR. Values are
mean±SEM. reports the dynamic
pressure-compliance (Figure 3A) and pressure-distensibility (Figure 3B)
relationships. For both carotid compliance and distensibility, there
was no significant difference between WKY and SHR, suggesting similar
dynamic behavior of the CCA in normotensive and hypertensive
strains.
View larger version (16K):
[in a new window]
Figure 3. Dynamic conditions: compliance (A) and
distensibility (B) of the in situ isolated CCA vs oscillatory
transmural pressure. indicates WKY; , SHR. Values are
mean±SEM. and 5 show the static and dynamic carotid
compliance (Figure 4A and 5A) and distensibility (Figure 4B and 5B)
with their respective static and dynamic strain values. Both
compliance- and distensibility-strain relationships are markedly
different between SHR and WKY either under static or dynamic
conditions, indicating stiffer material in hypertensive animals.
View larger version (15K):
[in a new window]
Figure 4. Static conditions: compliance (A) and
distensibility (B) of the in situ isolated CCA vs carotid wall strain.
indicates WKY; , SHR. Values are mean±SEM.
View larger version (14K):
[in a new window]
Figure 5. Dynamic conditions: compliance (A) and
distensibility (B) of the in situ isolated CCA vs carotid strain.
indicates WKY; , SHR. Values are mean±SEM.
CCA
=
common carotid artery
RF
=
radiofrequency
SHR
=
spontaneously hypertensive rats
WKY
=
Wistar-Kyoto rats
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