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1 Department of Mechanical Engineering and 2 Department of Neurology, The University of Vermont, Burlington, Vermont 05405
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Passive
(papaverine induced) and active (spontaneous pressure induced)
biomechanical properties of ischemic and nonischemic rat middle cerebral arteries (MCAs) were studied under pressurized conditions in vitro. Ischemic (1 h of occlusion),
contralateral, and sham-operated control MCAs were isolated from male
Wistar rats (n = 22) and pressurized using an
arteriograph system that allowed control of transmural pressure (TMP)
and measurement of lumen diameter and wall thickness. Three mechanical
stiffness parameters were computed: overall passive stiffness (
),
pressure-dependent modulus changes (Einc,p), and
smooth muscle cell (SMC) activity-dependent changes
(Einc,a). The -value for ischemic
vessels was increased compared with sham vessels (13.9 ± 1.7 vs.
9.1 ± 1.4, P < 0.05), indicating possible
short-term remodeling due to ischemia.
Einc,p increased with pressure in the passive
vessels (P < 0.05) but remained relatively constant in
the active vessels for all vessel types, indicating that
pressure-induced SMC contractile activity (i.e., myogenic reactivity)
in cerebral arteries leads to the maintenance of a constant elastic
modulus within the autoregulatory pressure range.
Einc,a increased with pressure for all
conditions, signifying that changes in stiffness are influenced by SMC
activity and vascular tone.
incremental elastic modulus; middle cerebral artery; vascular smooth muscle; myogenic reactivity
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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CEREBRAL ARTERIES function to supply oxygen and glucose to the brain, remove waste products, and regulate the ionic environment (17, 20). They also play an important role in the regulation of cerebral blood flow through autoregulation, a well-established phenomenon that is caused by a combination of myogenic, neuronal, and metabolic mechanisms (17, 23). Myogenic reactivity is the ability of the vascular smooth muscle cell (SMC) to contract in response to stretch or to an increase in transmural pressure (TMP) and to relax in response to a decrease in TMP (21). The myogenic response has been shown to contribute significantly to autoregulation in the cerebral circulation and provides a relatively constant blood flow even with large changes in arterial pressure (10, 27). Underlying the active response to pressure change is myogenic tone, a state of partial constriction of the vessel that provides a starting point from which an artery can modify its diameter and thus control cerebral blood flow (21). Many studies have documented the existence of myogenic tone in rat cerebral arteries and have found that autoregulation can begin at pressures as low as 40 mmHg and end at pressures as high as 180 mmHg (7, 12, 13, 25, 26, 28). Above this range, the vessels simply dilate with increases in pressure, a phenomenon known as forced dilatation (7).
It is this active constriction of arteries within the autoregulatory range that prompts studies of not just passive mechanical properties but also active mechanical properties. Passive properties provide an understanding of the behavior of the acellular extracellular matrix components of arteries (e.g., collagen and elastin); however, to understand how the artery behaves in vivo, it is necessary to understand mechanical properties with SMC activation. In addition, it is desirable to study cerebral vessels in their natural myogenic state rather than during drug-induced active states (e.g., KCl or norepinephrine) because the true autoregulatory efficiency of the myogenic mechanism is significantly decreased when the level of SMC activity increases above that due to intrinsic vascular tone (26). Thus pressure-induced SMC contraction gives a more physiological measure of active arterial mechanics compared with SMC contraction induced by pharmacological doses of vasoactive compounds. Mechanical properties might also be altered if the vessel is diseased or damaged. For example, ischemia has been shown to reduce vascular myogenic tone, which might lead to brain tissue damage during postischemic reperfusion by causing decreased vascular resistance and autoregulatory failure (2, 4-6). Therefore, studying the mechanical properties of vessels in disease states to determine whether they are able to adequately take part in controlling local blood flow may be important when considering therapeutic treatments such as thrombolysis (4).
Hayashi et al. (14) used a stiffness parameter () and
an incremental elastic modulus in their study of human intracranial and
extracranial cerebral arteries. These parameters have been shown to be
adequate measures of arterial stiffness and elasticity for many
different types of arteries, including human cerebral arteries, pig
thoracic aortas, and rabbit carotid arteries (11, 14-16,
24). In this study, we examined the mechanical properties of rat
middle cerebral arteries (MCAs) in their active (pressure activated)
and passive (papaverine induced) states. These arteries, like other
large cerebral arteries, operate in a state of partial constriction or
tone (2, 4-6, 17), which contributes significantly to
cerebrovascular resistance, and respond myogenically to changes in TMP
(2, 4-6, 17, 18). Therefore, the influence of
myogenic tone on the mechanical properties of cerebral arteries was
determined. In addition, data from MCAs exposed to ischemia and
reperfusion were analyzed to determine whether 1 h of
ischemia with 24 h of reperfusion has an effect on the
mechanical properties of the vessel wall. Parameters calculated from
the MCA pressure-diameter data include , an incremental elastic
modulus (Einc,p), and a modified incremental
modulus (Einc,a) that accounts for SMC
activation at different levels of TMP.
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MATERIALS AND METHODS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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MCA occlusion model. All procedures were approved by the Institutional Animal Care and Use Committee. Ischemia was produced by filament occlusion of the right MCA in male Wistar rats (weight 280-300 g) (2, 5, 22). The animals were anesthetized via an inhalation mask with halothane and oxygen. Body temperature was maintained at 37 ± 0.5°C with a heating pad and monitored with a rectal probe. The right carotid bifurcation was exposed, and the external carotid artery was coagulated distal to the bifurcation. After temporary ligature of the common carotid artery, a 5-0 nylon suture coated with silicon was inserted into the carotid artery through the external carotid artery stump and advanced through the internal carotid to occlude the origin of the MCA. The filament was carefully inserted just to the bifurcation of the MCA and anterior cerebral artery so as to avoid any mechanical disruption of the MCA (5). Laser-Doppler flowmetry was used to confirm successful occlusion and reperfusion. After 1 h of occlusion, the suture was removed to allow reperfusion, and the animal was allowed to recover. Animals were euthanized by anesthesia and decapitated 24 h after the suture was removed. Sham-operated control animals underwent anesthesia and a midline neck incision but no occlusion.
Preparation of arteries and pressurized arteriograph system. The MCA from both the right (occluded) and left (contralateral to ischemia) side of the brain was dissected, cleared of extraneous connective tissue, and placed in the arteriograph chamber. Dissected arteries were mounted on two glass microcannulas suspended above an optical window within the arteriograph chamber, perfused with physiological saline solution (PSS), and secured with two strands of nylon thread on both the proximal and distal cannulas. The distal cannula was closed off to flow, and a static TMP was applied to the vessels.
The arteriograph bath (Living Systems Instrumentation; Burlington, VT) consisted of two 20-ml fluid chambers with inlet and outlet ports for suffusion of PSS and drugs. PSS was continually recirculated and pumped through a heat exchanger to warm it to 37°C before it entered the arteriograph bath and was aerated with a gas mixture of 5% CO2-10% O2-85% N2 to maintain a constant pH of 7.4 ± 0.05. A servo system, which consisted of an in-line pressure transducer, miniature peristaltic pump, and controller connected to the proximal cannula, was used to measure and control TMP. The entire chamber that contained the mounted arteries was placed on an inverted microscope with an attached videocamera and monitor to allow viewing and electronic measurement of vessel dimensions. Lumen diameter and wall thickness were measured (±1.0 µm) by the video scan line, which detects the optical contrast of the vessel walls on the video monitor and generates a voltage ramp within the video dimension analyzer that is proportional to diameter (30). The output of the video dimension analyzer and pressure controller were sent to an IBM-compatible computer by means of a serial data-acquisition system (DATAQ) for visualization of dynamic responses of diameter and TMP.Experimental protocol. Mounted and pressurized arteries were equilibrated at a TMP of 50 mmHg for 1 h. Pressure was then increased stepwise in increments of 25 mmHg from 50 to 125 mmHg, and arterial diameter and wall thickness were recorded at each TMP once stable (~10 min). Active diameters were only determined within the myogenic range of 50-125 mmHg (17). In previous studies, these arteries have been shown to operate at 60-80% of systemic arterial pressure (17, 18). Once active data were obtained, papaverine (0.1 mmol/l), a compound that causes SMC relaxation, was added to the bath. This was used to obtain fully relaxed diameters and wall thickness measurements at each pressure from 0 to 200 mmHg.
Arteries studied were from two types of animals: sham-operated control (n = 7) and ischemic (n = 15). The three types of arteries studied were nonischemic sham, contralateral to ischemic, and ischemic. Calculations and statistical analysis were performed if complete data sets were available (i.e., if no diameter or wall thickness values were missing or indeterminate).Mechanical tissue property calculations For the purpose of this study, the rat MCA is considered to be a thick-walled cylindrical tube with orthotropic elasticity. The wall material is assumed to be incompressible, homogeneous, and globally nonlinear, but incrementally linear between neighboring states of deformation.
Because a thin wall assumption (ratio of wall thickness to internal radius <0.1) is not valid for these vessels, Laplace's equation is not an accurate calculation for determination of wall stress. Therefore, the circumferential stress (
) was
calculated at the inner and outer radius using the following equation
developed for a hollow cylinder submitted to uniform pressure
(29)
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) was calculated at the
internal and external radius using
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was calculated for the passive vessels using the
pressure-diameter data obtained over the entire pressure range
(0-200 mmHg). A regression was performed for each vessel using the
following equation (15)
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p is the incremental change in transmural pressure,
ri is the corresponding change in inner
radius, and ri, re, and p
are the internal radius, external radius, and pressure at the beginning
of the increment, respectively.
A modified incremental modulus was used to determine the effect
of SMC activity with increasing pressure because SMC activity alters
the mechanical properties of the arteries
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is the change in circumferential
stress (calculated at the internal radius) from passive to active,
ri is the change in internal radius from
passive to active, and the remaining terms are taken at the passive
vessel state.
Statistical analysis.
A repeated-measures ANOVA was performed on the
Einc,p and Einc,a data
using a program (BMDP 5V) that is capable of handling data containing
missing values for paired data. ANOVA was used to examine significant
differences among groups for -values, with a post hoc Bonferroni
test for multiple comparisons.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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The active, spontaneous constriction of the vessel at 75 mmHg was
apparent in all vessel types (Fig. 1),
indicative of myogenic behavior. The passive response, on the other
hand, showed a steady increase in diameter with increasing pressure
(Fig. 1). Also, the vessel diameters were noticeably smaller in the
active vessels, indicating the presence of myogenic tone.
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Circumferential stress-strain relationships were plotted for the active
and passive vessels over the entire range of pressures (Fig. 2,
A and B). Passive
vessels showed the "J"-shaped curve typically seen in arteries; an
exponential fit gave a good R2 value for all
passive vessel types (mean R2 = 0.99). In
contrast, the active vessels did not fit an exponential and displayed
an irregularly shaped curve due to the activity of the smooth muscle.
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The overall stiffness parameter , calculated for passive vessels,
was largest in the ischemic vessels (13.9 ± 1.7) and
smallest in the shams (9.1 ± 1.1) with P < 0.05 (Fig. 3). Contralateral vessels had
-values (10.2 ± 0.4) that were not significantly different
from sham or ischemic vessels. was only calculated for the
passive vessels because the active vessels did not have an exponential
pressure-diameter curve and thus gave a poor fit to the equation (mean
R2 < 0.55).
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Einc,p increased with increasing pressure for
all passive vessels (Fig. 4A)
but remained relatively constant in the active vessels (Fig.
4B). Passive values were also significantly higher than
active values at 125 mmHg (P < 0.05). Passive
incremental modulus values (106 dyn/cm2) at 75 mmHg were 5.6 ± 1.2, 5.3 ± 0.4, and 6.0 ± 1.0 compared with 14.7 ± 3.2, 35.5 ± 8.1, and 23.4 ± 5.1 at 125 mmHg for sham, contralateral, and ischemic vessels,
respectively. Active modulus values (106
dyn/cm2) at 75 mmHg were 6.2 ± 2.7, 4.5 ± 1.3, and 5.7 ± 1.6 compared with 6.9 ± 1.6, 5.6 ± 0.9, 10.0 ± 2.7 at 125 mmHg for sham, contralateral, and
ischemic vessels, respectively.
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Einc,a also increased for all vessel types with
increasing pressure, indicating that the SMC activity increased with
pressure (Fig. 5). Statistical analysis
revealed a highly significant change in Einc,a
over the four pressures (P < 0.001). Values
(106 dyn/cm2) at 50 mmHg were 7.3 ± 1.2, 10.7 ± 2.2, and 6.0 ± 0.9 and increased to 49.4 ± 12.6, 30.4 ± 4.4, and 36.6 ± 9.7 at 125 mmHg for sham, contralateral, and ischemic vessels, respectively.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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In this study, we used mechanical tissue property
measurements to study normal and ischemic MCAs in passive and
active states. Our results indicate that ischemic vessels were
stiffer than healthy vessels, which may be due to
ischemia-induced short-term remodeling. The overall stiffness
parameter was significantly higher in the ischemic vessels
than the sham-operated controls. The contralateral vessel stiffness,
although not significantly different than that in the sham or
ischemic vessels, tended to be more similar to the sham
vessels, indicating that the passive vessel stiffness changes were
limited to the ischemic vessels. This change in tissue mechanical behavior of the ischemic arteries suggests that some remodeling may be occurring in the passive arterial wall elements (e.g., increased collagen deposition).
The passive stress-strain relationship of blood vessels is nonlinear
due to the composite action of collagen and elastin found in both the
internal elastic lamina and media. The initial shallow slope is due to
the deformation of the highly extensible elastin fibers, and the
steepest portion is due to the recruitment of the stiffer collagen
fibers (20). The results of the stress-strain curves for
the passive vessels mirrored the results of the -calculations. As
seen in Fig. 2A, the sham vessels showed the most
distensibility. That is, for any given circumferential stress, the sham
vessels showed the greatest strain. The exponential fits to the data
also indicate that the ischemic vessels were the stiffest;
here, the highest exponential multiplier signifies the fastest increase and thus a steeper slope. Because neither the -calculation nor an
exponential fit to the stress-strain curve can be used to determine the
mechanical properties of the active vessels, comparisons between the
active and passive overall stiffness were not possible.
Einc,p, on the other hand, was calculated for all active and passive vessels (Fig. 4). This measurement of mechanical tissue behavior increased with pressure for all of the passive vessels but remained relatively constant for the active vessels. This result indicates that the passive vessels were increasingly stiff as pressure increased, whereas the SMC activity induced by pressure (i.e., myogenic reactivity) in the active vessels maintained a constant stiffness of the vessel wall. It is worth noting that at the two highest pressure increments, Einc,p for the passive contralateral vessels was larger than the other two groups and increased to a greater extent as pressure increased (Fig. 4A). Although there was not a significant difference in Einc,p among sham, contralateral, and ischemic groups at any of the pressure intervals, the greater value for contralateral vessels does suggest there may be a global effect of ischemia that is affecting the mechanical properties of contralateral arteries. Along these lines, we have recently shown an effect of postischemic reperfusion on the myogenic activity of contralateral arteries compared with nonischemic sham controls (2). Together, these results demonstrate that there may be a global effect of ischemia and reperfusion on both the functional (e.g., myogenic tone) and mechanical (e.g., Einc,p) properties of cerebral arteries.
Because there appears to be a global effect of ischemia on
cerebral artery structure and function, comparison to a
nonischemic control becomes important. In this study, we chose
to compare results to a sham-operated control, in which the animals
underwent anesthesia and midline neck incision but without any
occlusion of blood flow. This type of vessel controls for both
ischemia and procedures associated with surgery such as
anesthesia. However, in this study, the sham arteries were more
variable than the ischemic and contralateral arteries, possibly
because they were a completely different set of animals, whereas the
ischemic and contralateral arteries came from the same animals
and therefore had similar variability. This is evident in the
stress-strain curves shown in Fig. 2A, which show greater
variability in sham vessels compared with the other two groups. Whereas
this variability may be why the stress-strain curve for the
contralateral vessels are closer to the ischemic vessels but
the -values are closer to the sham group, the results are the same:
that the sham vessels are the most distensible and the least stiff.
It was also observed at higher pressures that active values for Einc,p were lower than the passive values. At first glance, this comparison suggests that SMC activity decreases stiffness compared with passive vessels at the higher pressures. However, the smaller modulus cannot be simply interpreted as a decrease in vessel stiffness with SMC activity. The decrease in diameter with SMC activity shifted the vessel down on the stress-strain curve (Fig. 2). In this region, the passive modulus or stiffness is lower, and the strain is also smaller. So, when the passive and active elastic moduli of vessels were compared at similar strains, the pressure-induced SMC activity actually contributed significant resistance to distension (1, 9).
The activation modulus Einc,a, developed to quantify the increase in stiffness with SMC activation, increased with higher pressures, as expected. This measure gives a direct indication of the contribution of the vascular SMC activity to stiffness at different pressures, unlike the somewhat complex comparison between active and passive Einc,p values. These results demonstrate that pressure-induced SMC activity in response to increased TMP (i.e., myogenic reactivity) increased the stiffness of the cerebral artery wall. The increased stiffness at higher pressures could contribute to autoregulation of cerebral blood flow by counteracting the increase in wall tension. Whether the pressure-induced increase in stiffness is due to increased force production (e.g., more actin-myosin interaction) or to active structural remodeling (e.g., SMC actin polyermerization), as has been suggested previously (3), is not clear from this study. However, the increased stiffness in response to increased TMP should be considered an important contributor to myogenic reactivity.
Full, three-dimensional constitutive modeling could not be performed based on these data because axial force and strain were not measured. However, vascular SMC activation acts principally in the circumferential direction and has little effect in the longitudinal direction (8). We also assumed that the MCA was radially and axially homogeneous, when in fact it has distinct layers in the radial direction. The active properties are dominated by vascular smooth muscle tone in contrast to the passive properties, which are influenced primarily by collagen and elastin (1). However, layer-specific information is not required to characterize the mechanical behavior of the tissue and our results reflect the bulk behavior of the MCAs.
In conclusion, this study calculated the mechanical properties of healthy and ischemic rat MCAs in both passive and active states. One hour of ischemia followed by 24 h of reperfusion did not appear to cause significant differences in the active mechanical response, but did alter the overall passive stiffness of the vessel. In addition, arterial wall elasticity was strongly influenced by the activity of vascular SMCs, which led to a relatively constant modulus of elasticity over the myogenic pressure range, demonstrating that pressure-induced constriction significantly increased the stiffness of the cerebral arterial wall.
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ACKNOWLEDGEMENTS |
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Graduate fellowship support (to R. J. Coulson) from the Vermont Experimental Program to Stimulate Competitive Research program is gratefully acknowledged. This project is based on work supported by National Science Foundation Faculty Early Career Development Program Grant 985012 (to N. C. Chesler), American Heart Association Beginning Grant-In-Aid 0060296 (to N. C. Chesler), and by National Center for Research Resources Centers for Biomedical Excellence Program Grant RR-15557 (to N. C. Chesler). Support was also through National Institute of Neurological Disorders and Stroke Grant 1-RO1-NS-40071 (to M. J. Cipolla). We also gratefully acknowledge the support of the Totman Medical Research Trust Fund.
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FOOTNOTES |
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Address for reprint requests and other correspondence: M. J. Cipolla, Dept. of Neurology, The Univ. of Vermont, Given Bldg., Rm. C454, 89 Beaumont Ave., Burlington, VT 05405 (E-mail: mcipolla{at}zoo.uvm.edu).
This article belongs to a collection of papers accepted in response to the Editor's special call for papers entitled "Mechanisms of vascular myogenic tone."
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
August 29, 2002;10.1152/ajpheart.00542.2002
Received 1 July 2002; accepted in final form 24 August 2002.
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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 F. Jimenez-Altayo, A. Martin, S. Rojas, C. Justicia, A. M. Briones, J. Giraldo, A. M. Planas, and E. Vila Transient middle cerebral artery occlusion causes different structural, mechanical, and myogenic alterations in normotensive and hypertensive rats Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H628 - H635. [Abstract] [Full Text] [PDF]
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G. Osol and J. Brayden Prologue: vascular myogenic mechanisms Am J Physiol Heart Circ Physiol, December 1, 2002; 283(6): H2157 - H2159. [Full Text] [PDF]
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