Mechanical properties of rat middle cerebral arteries with and without myogenic tone

The inner diameter and wall thickness of rat middle cerebral arteries (MCAs) were measured in vitro in both a pressure-induced, myogenically-active state and a drug-induced, passive state to quantify active and passive mechanical behavior. Elasticity parameters from the literature (stiffness derived from an exponential pressure-diameter relationship, beta, and elasticity in response to an increment in pressure, Einc-p) and a novel elasticity parameter in response to smooth muscle cell (SMC) activation, Einc-a, were calculated. beta for all passive MCAs was 9.11 +/- 1.07 but could not be calculated for active vessels. The incremental stiffness increased significantly with pressure in passive vessels; Einc-p (10(6) dynes/cm2) increased from 5.6 +/- 0.5 at 75 mmHg to 14.7 +/- 2.4 at 125 mmHg, (p < 0.05). In active vessels, Einc-p (10(6) dynes/cm2) remained relatively constant (5.5 +/- 2.4 at 75 mmHg and 6.2 +/- 1.0 at 125 mmHg). Einc-a (10(6) dynes/cm2) increased significantly with pressure (from 15.1 +/- 2.3 at 75 mmHg to 49.4 +/- 12.6 at 125 mmHg, p < 0.001), indicating a greater contribution of SMC activity to vessel wall stiffness at higher pressures.     

Effect of passive myocardium on the compliance of porcine coronary arteries

The objective of this study was to determine the effect of passive myocardium on the coronary arteries under distension and compression. To simulate distension and compression, we placed a diastolic-arrested heart in a Lucite box, where both the intravascular pressure and external (box) pressure were varied independently and expressed as a pressure difference (DeltaP = intravascular pressure - box pressure). The DeltaP-cross-sectional area relationship of the first several generations of porcine coronary arteries and the DeltaP-volume relationship of the coronary arterial tree (vessels >0.5 mm in diameter) were determined using a video densitometric technique in the range of +150 to -150 mmHg. The vasodilated left anterior descending (LAD) coronary artery of six KCl-arrested hearts were perfused with iodine and 3% Cab-O-Sil. The intravascular pressure was varied in a triangular pattern, whereas the absolute cross-sectional area of each vessel and the total arterial volume were calculated using video densitometry under different box pressures (0, 50, 100, and 150 mmHg). In the range of positive DeltaP, we found that the compliance of the proximal LAD artery in situ (4.85 +/- 3.8 x 10-3 mm2/mmHg) is smaller than that of the same artery in vitro (16.5 +/- 6 x 10-3 mm2/mmHg; P = 0.009). Hence, the myocardium restricts the compliance of the epicardial artery under distension. In the negative DeltaP range, the LAD artery does not collapse, whereas the same vessel readily collapses when tested in vitro. Hence, we conclude that myocardial tethering prevents collapse of large blood vessel under compression.     

Effects of biaxial stretch on arteriolar function in vitro

Mounting evidence suggests that the normal biomechanical state of arteries may include a nearly equibiaxial intramural stress and that arteries tend to undergo rapid and dramatic remodeling when perturbed from this normal state. Technical developments since the early 1980s have enabled in vitro (acute) and ex vivo (chronic culture) study of isolated, perfused microvessels, and it is clear that these vessels share many functional similarities with arteries. To date, however, there has been no systematic study of the effects of in-plane biaxial loading on the biomechanical behavior of arterioles. Here we describe a modification to a prior in vitro arterial test system that allowed us to investigate the role of altered axial stretch on the passive, myogenic, and norepinephrine-stimulated biaxial behavior of isolated rat cremaster arterioles. We show that axial stretches from 85% to 110% of values often used in the laboratory and consistent with those normally experienced in situ induce modest changes in the measured mean circumferential and axial stress-stretch behavior and in measures of distensibility and myogenic index. Nevertheless, altered axial stretch has a dramatic effect on the biaxial state of stress, and nearly equibiaxial stresses occur at axial stretches larger than those typically used in isolated arteriole studies. This finding is consistent with estimates of material and functional behavior in arterioles and suggests that long-term ex vivo studies, wherein vessel growth and remodeling are critical, should be performed at higher axial lengths than have been used during most prior in vitro tests.     

Effects of ischemia and myogenic activity on active and passive mechanical properties of rat cerebral arteries

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 (beta), pressure-dependent modulus changes (E(inc,p)), and smooth muscle cell (SMC) activity-dependent changes (E(inc,a)). The beta-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. E(inc,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. E(inc,a) increased with pressure for all conditions, signifying that changes in stiffness are influenced by SMC activity and vascular tone.     

Scaling of myocardial mass to flow and morphometry of coronary arteries.

There is no doubt that scaling relations exist between myocardial mass and morphometry of coronary vasculature. The purpose of this study is to quantify several morphological (diameter, length, and volume) and functional (flow) parameters of the coronary arterial tree in relation to myocardial mass. Eight normal porcine hearts of 117-244 g (mean of 177.5 +/- 32.7) were used in this study. Various coronary subtrees of the left anterior descending, right coronary, and left circumflex arteries were perfused at pressure of 100 mmHg with different colors of a polymer (Microfil) to obtain rubber casts of arterial trees corresponding to different regions of myocardial mass. Volume, diameter, and cumulative length of coronary arteries were reconstructed from casts to analyze their relationship to the perfused myocardial mass. Volumetric flow was measured in relationship with perfused myocardial mass. Our results show that arterial volume is linearly related to regional myocardial mass, whereas the sum of coronary arterial branch lengths, vessel diameters, and volumetric flow show an approximately 3/4, 3/8, and 3/4 power-law relationship, respectively, in relation to myocardial mass. These scaling laws suggest fundamental design principles underlying the structure-function relationship of the coronary arterial tree that may facilitate diagnosis and management of diffuse coronary artery disease.     

Systolic axial artery length reduction: an overlooked phenomenon in vivo

To demonstrate axial artery motion during the cardiac cycle, the common carotid arteries (CCA) of 10 pigs were exposed and equipped with piezoelectric crystals sutured onto the artery as axial position detectors. An echo-tracking system was used to simultaneously measure the CCA diameter. For each animal, data for pressure, length, and diameter were collected at a frequency of 457 Hz. At a mean pulse pressure of 33 +/- 8 mmHg, the mean systolodiastolic length difference was 0.3 +/- 0.01 mm for a mean arterial segment of 11.35 +/- 1.25 mm. Systolic and diastolic diameters were 4.1 +/- 0.3 and 3.9 +/- 0.2 mm, respectively. The examined CCA segment displayed a mean axial systolic shortening of 2.7%. This study clearly demonstrates, for the first time, that the length of a segment of the CCA changes during the cardiac cycle and that this movement is inversely correlated with pulse pressure. It is also apparent that the segmental axial strain is significantly smaller than the diameter variation during the cardiac cycle and that the impact of the axial strain for compliance computation should be further evaluated.     

Some unusual considerations about vessel walls and wall stresses

The "zero-stress state" of blood vessels is usually defined with respect to the atmospheric pressure p(a) ( approximately 750 mmHg). As a consequence, circumferential and axial wall stresses due to a positive transmural pressure can only be positive and thus, by definition, only tensile. If the zero-stress state were defined with respect to vacuum pressure (0 mmHg), the compressive stress -p(a) generated by p(a) everywhere in the wall would, however, be included so that negative (=compressive) wall stresses would formally become possible. In order to examine the consequences this alternative definition would have for arteries, we have compared radial, circumferential, and axial stresses calculated "conventionally" to the values they take when the zero-stress state is defined "correctly" by reference to the vacuum pressure. It turns out that, under normal physiologic conditions, axial stress and perhaps also circumferential stress might well be compressive in many elastic and conductance arteries, contrary to the intuitive conviction of many people. Since the type of stresses a vessel wall is submitted to may be highly relevant for its structure and mechanical properties, this unconventional way of considering wall stresses may reveal unsuspected relationships between wall stresses on one side, and wall structure, vessel growth, adaptation and repair processes, atherosclerosis, angioplasty or stenting on the other side. Similar considerations might also prove useful with regard to cardiac hypertrophy.     

Assessment of endothelial function of large, medium, and small vessels: a unified myograph

Endothelial dysfunction precedes the development of morphological atherosclerotic changes and can also contribute to lesion development in cardiovascular diseases. Currently, there is a lack of a single method to determine endothelial function of the entire range of vessel dimensions from aorta to arterioles. Here we assessed endothelial function of a large range of size arteries using a unified isovolumic myograph method. The method maintains a constant volume of fluid in the lumen of the vessel during contraction and relaxation, which are characterized by an increase and a decrease of pressure, respectively. Segments of six aortas, six common femoral arteries, and six mesenteric arteries from rats; six carotid arteries from mice; and six coronary and carotid arteries from pigs were used. The endothelium-dependent dose-response vasorelaxation was determined with endothelium-dependent vasodilators while arterial preconstriction was induced with vasoconstrictors at a submaximal dose. The circumferential midtension during vascular reactivity varied from 43.1 ± 7.9 to 2.59 ± 0.46 mN/mm (from large to small arteries), whereas the circumferential midstress showed a much smaller variation from 217 ± 23.5 to 123 ± 15.3 kPa (in the same range of vessels). We also found that overinflation and axial overelongation compromised endothelium-dependent vasorelaxation to underscore the significance of vessel preload. In conclusion, an isovolumic myograph was used to unify arterial vasoreactivity from large to small arteries and shows the uniformity of wall stress and %tension throughout the range of vessel sizes.     

Relaxin regulates vascular wall remodeling and passive mechanical properties in mice

Administration of recombinant human relaxin (rhRLX) to conscious rats increases global arterial compliance, and small renal arteries (SRA) isolated from these rats demonstrate increased passive compliance. Here we characterize relaxin-induced vascular remodeling and examine its functional relevance. SRA and external iliac arteries (EIA) were examined in rhRLX-treated (1.0 μg/h for 5 days) and relaxin knockout mice. Arterial geometric remodeling and compositional remodeling were quantified using immunohistochemical and biochemical techniques. Vascular mechanical properties were quantified using an ex vivo preparation wherein pressure-diameter data were obtained at various axial lengths. Compared with vehicle-treated mice, SRA from rhRLX-treated mice showed outward geometric remodeling (increased unstressed wall area and wall-to-lumen area ratio), increased smooth muscle cell (SMC) density, reduction in collagen-to-total protein ratio, and unchanged elastin-to-tissue dry weight ratio. Compared with wild-type mice, relaxin knockout mice exhibited the opposite pattern: decreased unstressed wall area and wall-to-lumen area ratio, decreased SMC density, and increased collagen-to-total protein ratio. Although tissue biaxial strain energy of SRA was not different between rhRLX- and vehicle-treated groups at low-to-physiological circumferential and axial strains, it was lower for the rhRLX-treated group at the highest circumferential strain. In contrast to SRA, relaxin administration was not associated with any vascular remodeling or changes in passive mechanics of EIA. Thus relaxin induces both geometric and compositional remodeling in vessel-specific manner. Relaxin-induced geometric remodeling of SRA is responsible for the increase in passive compliance under low-to-physiological levels of circumferential and axial strains, and compositional remodeling becomes functionally relevant only under high circumferential strain.     

Preliminary mechanical characterization of the small bowel for in vivo robotic mobility

In this work we present test methods, devices, and preliminary results for the mechanical characterization of the small bowel for intra luminal robotic mobility. Both active and passive forces that affect mobility are investigated. Four investigative devices and testing methods to characterize the active and passive forces are presented in this work: (1) a novel manometer and a force sensor array that measure force per cm of axial length generated by the migrating motor complex, (2) a biaxial test apparatus and method for characterizing the biomechanical properties of the duodenum, jejunum, and ileum, (3) a novel in vitro device and protocol designed to measure the energy required to overcome the self-adhesivity of the mucosa, and (4) a novel tribometer that measures the in vivo coefficient of friction between the mucus membrane and the robot surface. The four devices are tested on a single porcine model to validate the approach and protocols. Mean force readings per cm of axial length of intestine that occurred over a 15?min interval in vivo were 1.34?±?0.14 and 1.18?±?0.22?N cm(-1) in the middle and distal regions, respectively. Based on the biaxial stress/stretch tests, the tissue behaves anisotropically with the circumferential direction being more compliant than the axial direction. The mean work per unit area for mucoseparation of the small bowel is 0.08?±?0.03 mJ cm(-2). The total energy to overcome mucoadhesion over the entire length of the porcine small bowel is approximately 0.55?J. The mean in vivo coefficient of friction (COF) of a curved 6.97 cm(2) polycarbonate sled on live mucosa traveling at 1?mm s(-1) is 0.016?±?0.002. This is slightly lower than the COF on excised tissue, given the same input parameters. We have initiated a comprehensive program and suite of test devices and protocols for mechanically characterizing the small bowel for in vivo mobility. Results show that each of the four protocols and associated test devices has successfully gathered preliminary data to confirm the validity of our test approach.     

Gender differences in biomechanical properties of intramural coronary resistance arteries of rats, an in vitro microarteriographic study

The prevalence of ischemic heart disease is lower in premenopausal females than in males of corresponding age. This should be related to gender differences in coronary functions. We tested whether biomechanical differences exist between intramural coronary resistance arteries of male and female rats. Intramural branches of the left anterior descending coronary artery (uniformly approximately 200microm in diameter) were isolated, cannulated and studied by microarteriography. Intraluminal pressure was increased from 2 to 90mmHg in steps and steady-state diameters were measured. Measurements were repeated in the presence of vasoconstrictor U46619 (10(-6)M) and the endothelial coronary vasodilator bradykinin (BK) (10(-6)M). Finally, passive diameters were recorded in calcium-free saline. A similar inner radius and a higher wall thickness (41.5+/-2.9microm vs. 31.4+/-2.7microm at 50mmHg in the passive condition, p<0.05) resulted in lower tangential wall stresses in male rats (18.9+/-1.9kPa vs. 24.9+/-2.5kPa at 50mmHg, p<0.05). Isobaric elastic modulus of vessels from male animals was significantly smaller at higher pressures. Vasoconstrictor response was significantly stronger in male than in female animals. Endothelial relaxations induced by BK were not different. This is the first demonstration that biomechanical characteristics of intramural coronary resistance arteries of a mammalian species are different in the male and female sexes. Higher wall thickness and higher vascular contractility in males are associated with similar endothelial function and larger high-pressure elasticity compared to females. These gender differences in biomechanics of coronary resistance arteries of rats may contribute to our better understanding the characteristic physiological and pathological differences in humans.     

Myocardial blood volume and coronary resistance during and after coronary angioplasty

Animal experiments have shown that the coronary circulation is pressure distensible, i.e., myocardial blood volume (MBV) increases with perfusion pressure. In humans, however, corresponding measurements are lacking so far. We sought to quantify parameters reflecting coronary distensibility such as MBV and coronary resistance (CR) during and after coronary angioplasty. Thirty patients with stable coronary artery disease underwent simultaneous coronary perfusion pressure assessment and myocardial contrast echocardiography (MCE) of 37 coronary arteries and their territories during and after angioplasty. MCE yielded MBV and myocardial blood flow (MBF; in ml · min(-1) · g(-1)). Complete data sets were obtained in 32 coronary arteries and their territories from 26 patients. During angioplasty, perfusion pressure, i.e., coronary occlusive pressure, and MBV varied between 9 and 57 mmHg (26.9 ± 11.9 mmHg) and between 1.2 and 14.5 ml/100 g (6.7 ± 3.7 ml/100 g), respectively. After successful angioplasty, perfusion pressure and MBV increased significantly (P < 0.001 for both) and varied between 64 and 118 mmHg (93.5 ± 12.8 mmHg) and between 3.7 and 17.3 ml/100 g (9.8 ± 3.4 ml/100 g), respectively. Mean MBF increased from 31 ± 20 ml · min(-1) · g(-1) during coronary occlusion, reflecting collateral flow, to 121 ± 33 ml · min(-1) · g(-1) (P < 0.01), whereas mean CR, i.e., the ratio of perfusion pressure and MBF, decreased by 20% (P < 0.001). In conclusion, the human coronary circulation is pressure distensible. MCE allows for the quantification of CR and MBV in humans.     

Deformation-induced endothelin B receptor-mediated smooth muscle cell apoptosis is matrix-dependent

To maintain normal blood flow, pressure overload in both arteries and veins requires a structural adaptation of the vessel wall (remodelling) that involves smooth muscle cell (SMC) hypertrophy and/or hyperplasia. Due to its potent vasoconstrictor and growth-promoting effects, endothelin-1 (ET-1) is a likely candidate to initiate and/or promote remodelling in blood vessels exposed to a chronic increase in blood pressure. To test this hypothesis, isolated segments of the rabbit carotid artery and jugular vein were perfused at different levels of intraluminal pressure. In both types of segments, pressure overload (160 and 20 mmHg, respectively) resulted in an increase in endothelial prepro-ET-1 and SMC endothelin B receptor (ETB-R) expression. Moreover, in pressurised segments from the carotid artery an ETB-R antagonist-sensitive increase in SMC apoptosis in the media was observed, while in the vein medial SMC started to proliferate. Isolated SMC from these rabbit blood vessels as well as from the aorta and vena cava of the rat, when cultured on a collagen or laminin matrix, uniformly revealed an ETB-R-mediated increase in apoptosis upon exposure to mechanical deformation plus exogenous ET-1 (10 nmol/L). However, when grown on a fibronectin matrix, the cultured SMC did not respond with an increase in apoptosis under otherwise identical experimental conditions. These findings suggest that deformation-induced activation of the endothelin system in the vessel wall not only plays a crucial role in remodelling, but that the structural components of the vessel wall, in particular the cell-matrix interaction, determine how SMC respond phenotypically to these changes in gene expression.     

Rho kinase inhibition partly weakens myogenic reactivity in rat small arteries by changing calcium sensitivity

The hypothesis that Rho kinase is involved in myogenic reactivity was investigated in pressurized rat tail small arteries using videomicroscopic diameter determination and calcium fluorimetry. The potent Rho kinase inhibitor Y-27632 reversibly increased vessel diameter at 80 mmHg without changing the intracellular calcium concentration ([Ca](i)) shifting the relationship between diameter change and [Ca](i) to higher calcium levels. Neither endothelium removal nor inhibition of neural transmission affected the Y-27632-induced effect. Y-27632 at 3 x 10(-6) mol/l attenuated the myogenic response in the pressure range from 10 to 120 mmHg, shifting the relationship between vessel tone and [Ca](i) to higher calcium levels. In addition, the Y-27632-induced shift of the relationship between vessel tone and [Ca](i) was larger at 80 than at 10 mmHg. These results suggest that smooth muscle cell Rho kinase in rat tail small arteries 1) is in an active state partly determining the level of the myogenic tone, and 2) alters the strength of the myogenic response by changing calcium sensitivity, probably caused by the pressure-induced activation of the kinase.     

Three-dimensional mechanical properties of porcine coronary arteries: a validated two-layer model

The normal coronary artery consists of two mechanically distinct layers: intima-media and adventitia. The objective of this study is to establish a two-layer three-dimensional (3-D) stress-strain relation of porcine coronary arteries. Experimental measurements were made by a series of biaxial tests (inflation and axial extension) of intact coronary arteries and, subsequently, their corresponding intima-media or adventitia layer. The Fung-type exponential strain energy function was used to describe the 3-D strain-stress relation for each layer and the intact wall. A genetic algorithm was used to determine the material constants in the Fung-type constitutive equation by curve fitting the experimental data. Because one layer must be sacrificed before the other layer can be tested, the material property of the missing layer was computed from the material constants of the intact vessel and the tested layer. A total of 20 porcine hearts were used: one group of 10 hearts for the left anterior descending artery and another group of 10 hearts for the right coronary artery. Each group was further divided into two subgroups of five specimens tested for the intact wall and the intima-media layer and for the intact wall and the adventitia layer. Our results show statistically significant differences in the material properties of the two layers. The mathematical model was validated by experimental stress-strain data for individual layers. The validated 3-D constitutive model will serve as a foundation for formulation of layer-specific boundary value problems in coronary physiology and cardiology.     

Measurements of mouse pulmonary artery biomechanics

BACKGROUND: Robust techniques for characterizing the biomechanical properties of mouse pulmonary arteries will permit exciting gene-level hypotheses regarding pulmonary vascular disease to be tested in genetically engineered animals. In this paper, we present the first measurements of the biomechanical properties of mouse pulmonary arteries. METHOD OF APPROACH: In an isolated vessel perfusion system, transmural pressure, internal diameter and wall thickness were measured during inflation and deflation of mouse pulmonary arteries over low (5-40 mmHg) and high (10-120 mmHg) pressure ranges representing physiological pressures in the pulmonary and systemic circulations, respectively. RESULTS: During inflation, circumferential stress versus strain showed the nonlinear "J"-shape typical of arteries. Hudetz's incremental elastic modulus ranged from 27 +/- 13 kPa (n = 7) during low-pressure inflation to 2,700 +/- 1,700 kPa (n = 9) during high-pressure inflation. The low and high-pressure testing protocols yielded quantitatively indistinguishable stress-strain and modulus-strain results. Histology performed to assess the state of the tissue after mechanical testing showed intact medial and adventitial architecture with some loss of endothelium, suggesting that smooth muscle cell contractile strength could also be measured with these techniques. CONCLUSIONS: The measurement techniques described demonstrate the feasibility of quantifying mouse pulmonary artery biomechanical properties. Stress-strain behavior and incremental modulus values are presented for normal, healthy arteries over a wide pressure range. These techniques will be useful for investigations into biomechanical abnormalities in pulmonary vascular disease.     

Impact of Short-Term Treatment with Telmisartan on Cerebral Arterial Remodeling in SHR

Background and Purpose

Chronic hypertension decreases internal diameter of cerebral arteries and arterioles. We recently showed that short-term treatment with the angiotensin II receptor blocker telmisartan restored baseline internal diameter of small cerebral arterioles in spontaneously hypertensive rats (SHR), via reversal of structural remodeling and inhibition of the angiotensin II vasoconstrictor response. As larger arteries also participate in the regulation of cerebral circulation, we evaluated whether similar short-term treatment affects middle cerebral arteries of SHR.

Methods

Baseline internal diameters of pressurised middle cerebral arteries from SHR and their respective controls, Wistar Kyoto rats (WKY) and responses to angiotensin II were studied in a small vessel arteriograph. Pressure myogenic curves and passive internal diameters were measured following EDTA deactivation, and elastic modulus from stress-strain relationships.

Results

Active baseline internal diameter was 23% lower in SHR compared to WKY, passive internal diameter (EDTA) 28% lower and elastic modulus unchanged. Pressure myogenic curves were shifted to higher pressure values in SHR. Telmisartan lowered blood pressure but had no effect on baseline internal diameter nor on structural remodeling (passive internal diameter and elastic modulus remained unchanged compared to SHR). Telmisartan shifted the pressure myogenic curve to lower pressure values than SHR.

Conclusion

In the middle cerebral arteries of SHR, short-term treatment with telmisartan had no effect on structural remodeling and did not restore baseline internal diameter, but allowed myogenic tone to adapt towards lower pressure values.     

Biomechanical properties of decellularized porcine common carotid arteries

To analyze the effects of decellularization on the biomechanical properties of porcine common carotid arteries, decellularization was performed by a detergent-enzymatic procedure that preserves extracellular matrix scaffold. Internal diameter, external diameter, and wall thickness were measured by optical microscopy on neighboring histological sections before and after decellularization. Rupture tests were conducted. Inner diameter and wall thickness were measured by echo tracking during pressure inflation from 10 to 145 mmHg. Distensibility and incremental elastic modulus were computed. At 10 mmHg, mean diameter of decellularized arteries was 5.38 mm, substantially higher than controls (4.1 mm), whereas decellularized and control arteries reached the same internal diameter (6.7 mm) at 145 mmHg. Wall thickness decreased 16% for decellularized and 32% for normal arteries after pressure was increased from 10 to 145 mmHg. Decellularized arteries withstood pressure >2,200 mmHg before rupture. At 145 mmHg, decellularization reduced compliance by 66% and increased incremental elastic modulus by 54%. Removal of cellular elements from media led to changes in arterial dimensions. Collagen fibers engaged more rapidly during inflation, yielding a stiffer vessel. Distensibility was therefore significantly lower (by a factor of 3) in decellularized than in normal vessels: reduced in the physiological range of pressures. In conclusion, decellularization yields vessels that can withstand high inflation pressures with, however, markedly different geometrical and biomechanical properties. This may mean that the potential use of a decellularized artery as a scaffold for the creation of xenografts may be compromised because of geometrical and compliance mismatch.     

A multiaxial computer-controlled organ culture and biomechanical device for mouse carotid arteries

Much of our understanding of vascular mechanotransduction has come from studies using either cell culture or in vivo animal models, but the recent success of organ culture systems offers an exciting alternative. In studying cell-mediated vascular adaptations to altered loading, organ culture allows one to impose well-controlled mechanical loads and to perform multiaxial mechanical tests on the same vessel throughout the culture period, and thereby to observe cell-mediated vascular adaptations independent of neural and hormonal effects. Here, we present a computer-controlled perfused organ culture and biomechanical testing device designed for small caliber (50-5000 micron) blood vessels. This device can control precisely the pulsatile pressure, luminal flow, and axial load (or stretch) and perform intermittent biaxial (pressure-diameter and axial load-length) and functional tests to quantify adaptations in mechanical behavior and cellular function, respectively. Device capabilities are demonstrated by culturing mouse carotid arteries for 4 days.