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Effects of clonidine on aortic pressure-diameter and elastic stiffness-stress relations in anaesthetized rabbits.

1. The effects of clonidine on the aortic pressure-diameter relationship were studied in anaesthetized rabbits by means of an ultrasonic dimension technique. Midwall aortic stress and aortic elastic modulus were calculated. 2. In spite of a significant decrease in mean aortic blood pressure, aortic diameter was slightly but not significantly increased after intravenous clonidine injection (25 microgram/kg body wt., intravenously over 30 s). 3. Midwall aortic stress was decreased when compared at the same aortic radius and aortic elastic modulus was increased when compared at a common blood pressure level. However, when aortic elastic modulus was plotted as a linear function of the stress, no difference was observed before and after clonidine. 4. The results suggest that the pressure-diameter changes induced by clonidine were primarily reflecting the mechanical changes in the aortic wall due to changes in smooth muscle tension. Furthermore it seems that the elastic modulus of the aorta tends to remain constant by adaptive changes in the aortic wall which over-ride the concurrent geometrical changes to maintain a level of elasticity consistent with the degree of aortic stress.

Animals↗

Short-term variation in the elastic properties of a muscular artery in humans.

1. Information on the interaction between mechanical strain and the elastic properties of large arteries could give insight to the origin of haemodynamic vascular injury, possibly resulting in formation of atherosclerotic plaques. Intra-individual variation in the elastic properties of muscular arteries measured using non-invasive techniques has been observed. This variation could be due to changes in blood pressure, since the elastic properties of muscular arteries are strongly non-linear. 2. The objective of the present study was to evaluate variability in the elastic properties of a muscular artery over a time period of up to 1 h. Furthermore, the relation between changes in elastic properties and alterations in blood pressure was studied. With a non-invasive high-resolution ultrasound technique, the diameter and distension of the femoral artery were assessed by repeated measurements in 10 healthy subjects (mean age 27 +/- 2.9 years) under resting conditions over 40-60 min. Intra-arterial blood pressure of the contralateral common femoral artery and heart rate were recorded simultaneously. From the distension and pulse pressure, the distension/pressure ratio was calculated, a measure of the compliance. For each parameter the variation coefficient was computed. 3. In all subjects a considerable variation was found in distension (mean variation coefficient 14.8%) but not in pulse pressure (mean variation coefficient 3.7%). The expected positive correlation between pulse pressure and distension was absent in eight subjects. As a consequence, large intra-individual variation was found in the distension/pressure ratio (mean variation coefficient 15.3%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

All-trans retinoic acid promotes the repair of tortuosity of elastic fibres in rat skin.

To elucidate the repair effects of all-trans retinoic acid (t-RA) on ultraviolet (UV)-induced tortuosity of elastic fibres in rat skin, the hind limbs of Sprague-Dawley rats were irradiated at a suberythemal dose of UV (three times/week for 6 weeks) and 0.025% t-RA in ethanol was applied topically five times/week for 6 weeks. The three-dimensional arrangement of elastic fibres with special reference to their linearity was quantified by image analysis using a scanning electron microscope following a combination of intravascular resin injection and selective digestion using formic acid. When t-RA was topically applied for 6 weeks on wrinkles formed by 6 weeks' exposure of the skin of rat hind limbs to UV radiation, the wrinkles disappeared to control levels, concomitant with an improvement in skin elasticity. The linearity of the elastic fibres was significantly (P < 0.01) increased compared with age-matched UV-irradiated controls. These findings suggest that the degeneration and deposition of elastic fibres accompanied by an increase in their linearity is involved in the process of wrinkle repair by topical application of t-RA.

Administration, Topical↗

An evaluation of acrylic complete dentures using the discrimination of elastic bodies or viscous fluids.

The discrimination test on elastic bodies and viscous fluids was carried out for 16 young dentists and 13 denture patients, because it is considered that dentures affect the ability to discriminate food. The materials used in this test were six thermoplastic polyurethane elastomers with compressive elastic moduli from 11.8 to 62.0 MPa and six silicone impression pastes with coefficients of viscosity from 1.77 x 10(-2) to 23.0 x 10(-2) MPa x s. The subjects (dentists and patients) discriminated the materials based on differences in elastic moduli or coefficients of viscosity by chewing the materials for 10 s. From these experiments, it became clear that the ability to discriminate between elastic bodies or viscous fluids upon chewing, of subjects who use complete-dentures in combination with their own teeth and either an upper or lower complete-denture (S/D) or who have a set of complete-dentures in both jaws (D/D) decreased considerably, compared with that of subjects who have their own teeth in upper and lower jaws (S/S). The ratios of S/D and D/D against S/S were 0.5 and 0.3, respectively. This indicates that with an increase in the area occupied by dentures in the oral cavity, the value of the differential threshold increased markedly and made food discrimination more difficult. In addition, discriminating viscous fluids was 2.4 to 3.1 times more difficult compared with the discrimination of elastic bodies, independent of denture placement.

Acrylic Resins↗

Changes of the elastic fibre network of the rabbit temporomandibular joint following discectomy.

Elastic fibres are thought to be very important for the function of various organs including the temporomandibular joint (TMJ). The current study was designed to examine changes in the elastic fibres of the TMJ following discectomy. The TMJs of six rabbits were surgically exposed, and the disc removed with a scalpel. Three untreated and three sham-operated rabbits were used as controls. Complete TMJs were removed in three rabbits 1 month and in three rabbits 3 months after discectomy and processed for histochemical demonstration of elastic fibres. In the TMJ 1 month after discectomy, osteoarthritic changes and a significant increase in the numbers of elastic fibres were observed in the condyle and articular eminence. In the TMJs 3 months after discectomy, they tended to revert to the levels in the condyle and articular eminence of the control TMJs. Our results show that after experimental discectomy, elastic fibres very often appear initially in the condyle and articular eminence, but they are destined to disappear later. This information may improve our understanding of the consequences of removal of the disc in clinical practice.

Animals↗

An experimental study of a new sutureless intraluminal graft with an elastic ring that can attach itself to the vessel wall. A preliminary report.

A new sutureless intraluminal graft was developed with an elastic ring made of a flat spring. The diameter of the ring could be reversibly reduced by compression. The sutureless intraluminal graft with an elastic ring can attach itself to the vessel wall by elastic expansion of the ring. The elastic-ring graft was implanted in the descending thoracic aortas of nine dogs and was evaluated histologically and angiographically at different intervals from 18 to 150 days. No complication such as detachment of the ring, aortic rupture, stenosis, or aneurysmal dilatation was observed. With the new graft neither ligation nor posterior aortic wall dissection is necessary, and no anastomotic stenosis occurs. This graft is applicable even if the diameter of the aorta is small. Therefore the elastic-ring sutureless intraluminal graft promises theoretic advantages over sutureless methods that use tape ligation.

Animals↗

Series elasticity in frog muscle as revealed by optical diffraction.

Using an optical diffraction technique, the series elasticity of frog striated muscle fibres was investigated. One source of series elasticity was located in the cross-bridges during the application of either quick stretches or releases of muscle fibres. Evidence is presented here for a second component attributable to a small population of slowly activated sarcomeres. The size of the second component was progressively reduced until it virtually disappeared at a sarcomere length of 3 microns. A third component appears to reside in the thick filaments. Calculation of the elastic energy in the muscle fibres enabled an identification of the source of the energy to be made in terms of the components of the series elasticity. Evidence is presented of a short-range elastic component present in resting fibres.

Animals↗

Damped elastic recoil of the titin spring in myofibrils of human myocardium.

The giant protein titin functions as a molecular spring in muscle and is responsible for most of the passive tension of myocardium. Because the titin spring is extended during diastolic stretch, it will recoil elastically during systole and potentially may influence the overall shortening behavior of cardiac muscle. Here, titin elastic recoil was quantified in single human heart myofibrils by using a high-speed charge-coupled device-line camera and a nanonewtonrange force sensor. Application of a slack-test protocol revealed that the passive shortening velocity (Vp) of nonactivated cardiomyofibrils depends on: (i) initial sarcomere length, (ii) release-step amplitude, and (iii) temperature. Selective digestion of titin, with low doses of trypsin, decelerated myofibrillar passive recoil and eventually stopped it. Selective extraction of actin filaments with a Ca2+-independent gelsolin fragment greatly reduced the dependency of Vp on release-step size and temperature. These results are explained by the presence of viscous forces opposing myofibrillar passive recoil that are caused mainly by weak actin-titin interactions. Thus, Vp is determined by two distinct factors: titin elastic recoil and internal viscous drag forces. The recoil could be modeled as that of a damped entropic spring consisting of independent worm-like chains. The functional importance of myofibrillar elastic recoil was addressed by comparing instantaneous Vp to unloaded shortening velocity, which was measured in demembranated, fully Ca2+-activated, human cardiac fibers. Titin-driven passive recoil was much faster than active unloaded shortening velocity in early phases of isotonic contraction. Damped myofibrillar elastic recoil could help accelerate active contraction speed of human myocardium during early systolic shortening.

Actins↗

Regulation of skeletal muscle stiffness and elasticity by titin isoforms: a test of the segmental extension model of resting tension.

To explore the role of titin filaments in muscle elasticity, we measured the resting tension-sarcomere length curves of six rabbit skeletal muscles that express three size classes of titin isoform. The stress-strain curves of the split fibers of these muscles displayed a similar multiphasic shape, with an exponential increase in tension at low sarcomere strain followed by a leveling of tension and a decrease in stiffness at and beyond an elastic limit (yield point) at higher sarcomere strain. Significantly, positive correlations exist between the size of the expressed titin isoform, the sarcomere length at the onset of exponential resting tension, and the yield point of each muscle. Immunoelectron microscopic studies of an epitope in the extensible segment of titin revealed a transition in the elastic behavior of the titin filaments near the yield point sarcomere length of these muscles, providing direct evidence of titin's involvement in the genesis of resting tension. Our data led to the formulation of a segmental extension model of resting tension that recognizes the interplay of three major factors in shaping the stress-strain curves: the net contour length of an extensible segment of titin filaments (between the Z line and the ends of the thick filaments), the intrinsic molecular elasticity of titin, and the strength of titin thick filament anchorage. Our data further suggest that skeletal muscle cells may control and modulate stiffness and elastic limit coordinately by selective expression of specific titin isoforms.

Animals↗

Nature of PEVK-titin elasticity in skeletal muscle.

A unique sequence within the giant titin molecule, the PEVK domain, has been suggested to greatly contribute to passive force development of relaxed skeletal muscle during stretch. To explore the nature of PEVK elasticity, we used titin-specific antibodies to stain both ends of the PEVK region in rat psoas myofibrils and determined the region's force-extension relation by combining immunofluorescence and immunoelectron microscopy with isolated myofibril mechanics. We then tried to fit the results with recent models of polymer elasticity. The PEVK segment elongated substantially at sarcomere lengths above 2.4 micro(m) and reached its estimated contour length at approximately 3.5 micro(m). In immunofluorescently labeled sarcomeres stretched and released repeatedly above 3 micro(m), reversible PEVK lengthening could be readily visualized. At extensions near the contour length, the average force per titin molecule was calculated to be approximately 45 pN. Attempts to fit the force-extension curve of the PEVK segment with a standard wormlike chain model of entropic elasticity were successful only for low to moderate extensions. In contrast, the experimental data also could be correctly fitted at high extensions with a modified wormlike chain model that incorporates enthalpic elasticity. Enthalpic contributions are likely to arise from electrostatic stiffening, as evidenced by the ionic-strength dependency of titin-based myofibril stiffness; at high stretch, hydrophobic effects also might become relevant. Thus, at physiological muscle lengths, the PEVK region does not function as a pure entropic spring. Rather, PEVK elasticity may have both entropic and enthalpic origins characterizable by a polymer persistence length and a stretch modulus.

Animals↗

Impaired elastic-fiber assembly by fibroblasts from patients with either Morquio B disease or infantile GM1-gangliosidosis is linked to deficiency in the 67-kD spliced variant of beta-galactosidase.

We have previously shown that intracellular trafficking and extracellular assembly of tropoelastin into elastic fibers is facilitated by the 67-kD elastin-binding protein identical to an enzymatically inactive, alternatively spliced variant of beta-galactosidase (S-Gal). In the present study, we investigated elastic-fiber assembly in cultures of dermal fibroblasts from patients with either Morquio B disease or GM1-gangliosidosis who bore different mutations of the beta-galactosidase gene. We found that fibroblasts taken from patients with an adult form of GM1-gangliosidosis and from patients with an infantile form, carrying a missense mutations in the beta-galactosidase gene-mutations that caused deficiency in lysosomal beta-galactosidase but not in S-Gal-assembled normal elastic fibers. In contrast, fibroblasts from two cases of infantile GM1-gangliosidosis that bear nonsense mutations of the beta-galactosidase gene, as well as fibroblasts from four patients with Morquio B who had mutations causing deficiency in both forms of beta-galactosidase, did not assemble elastic fibers. We also demonstrated that S-Gal-deficient fibroblasts from patients with either GM1-gangliosidosis or Morquio B can acquire the S-Gal protein, produced by coculturing of Chinese hamster ovary cells permanently transected with S-Gal cDNA, resulting in improved deposition of elastic fibers. The present study provides a novel and natural model validating functional roles of S-Gal in elastogenesis and elucidates an association between impaired elastogenesis and the development of connective-tissue disorders in patients with Morquio B disease and in patients with an infantile form of GM1-gangliosidosis.

Alternative Splicing↗

Long-term thyrotropin-suppressive therapy with levothyroxine impairs small and large artery elasticity and increases left ventricular mass in patients with thyroid carcinoma.

BACKGROUND: Exogenous subclinical hyperthyroidism, caused by long-term thyrotropin (TSH)-suppressive treatment with levothyroxine (LT(4)), is associated with several cardiovascular abnormalities. In order to assess the effect of long-term thyroid hormone-suppressive therapy on the blood vessels and myocardium, we determined the arterial elasticity, using the pulse wave contour analysis. METHODS AND RESULTS: Twenty-six athyreotic patients receiving TSH-suppressive LT(4) therapy for periods ranging from 3 to 21 years at a mean daily dose of 2.25 +/- 0.5 microg/kg per day were included in the study. Twenty six age- and gender-matched healthy subjects served as controls. Arterial elasticity of large and small arteries was evaluated using pulse wave contour analysis method (HDI CR 200, Eagen, MN). Cardiac structure was assessed by two-dimensional echocardiography. We found decreased large artery elasticity in subclinical hyperthyroidism (sHT) patients compared to controls (14.14 +/- 3.38 versus 10.53 +/- 2.43 L/mm Hg x 100, p < 0.000). Small artery elasticity was also lower in patients than in controls (5.42 +/- 1.82 versus 4.30 +/- 1.75 mL/mm Hg x 100, p < 0.056). The echocardiographic data showed significantly increased left ventricular (LV) mass index (101.90 +/- 18.61 versus 88.03 +/- 22.01 g/m(2), p < 0.049) and interventricular septum thickness (10.61 +/- 1.46 versus 9.11 +/- 1.13 mm, p < 0.002) in LT(4)-treated patients compared to controls. CONCLUSIONS: We found impaired vascular elasticity of large and small arteries and increased LV mass in patients receiving long-term TSH-suppressive therapy with LT(4).

Arteries↗

Characterization of an in vitro model of elastic fiber assembly.

Elastic fibers consist of two morphologically distinct components: elastin and 10-nm fibrillin-containing microfibrils. During development, the microfibrils form bundles that appear to act as a scaffold for the deposition, orientation, and assembly of tropoelastin monomers into an insoluble elastic fiber. Although microfibrils can assemble independent of elastin, tropoelastin monomers do not assemble without the presence of microfibrils. In the present study, immortalized ciliary body pigmented epithelial (PE) cells were investigated for their potential to serve as a cell culture model for elastic fiber assembly. Northern analysis showed that the PE cells express microfibril proteins but do not express tropoelastin. Immunofluorescence staining and electron microscopy confirmed that the microfibril proteins produced by the PE cells assemble into intact microfibrils. When the PE cells were transfected with a mammalian expression vector containing a bovine tropoelastin cDNA, the cells were found to express and secrete tropoelastin. Immunofluorescence and electron microscopic examination of the transfected PE cells showed the presence of elastic fibers in the matrix. Biochemical analysis of this matrix showed the presence of cross-links that are unique to mature insoluble elastin. Together, these results indicate that the PE cells provide a unique, stable in vitro system in which to study elastic fiber assembly.

Animals↗

Anti-atherosclerotic action of elastase--with special reference to its effect on elastic fibres.

In order to determine the anti-atherosclerotic action of elastase, the aortas from four groups of rats--group N fed a normal diet, group D fed an atherogenic diet with vitamin D2, group N + Ela fed a normal diet with elastase, and group D + Ela fed an atherogenic diet and vitamin D2 with elastase--were studied histologically after 3, 6, 9, and 12 weeks of feeding. Group D displayed a remarkable atheromatous change, while the change was insignificant in group D + Ela. The histopathological findings in group D consisted of marked rarefaction, fat deposition, and atheroma in the subendothelial tissue and tunica intima; Van Gieson's staining revealed a conspicuous decrease in elastic fibres, and the remaining elastic fibres had such abnormalities as a tortuous course, bends, and fissures. For group D + Ela, on the other hand, there were few foam cells in the subendothelial tissue and tunica intima and much less marked rarefaction of interstice and fat deposition. Further, the arrangement of elastic fibres was only slightly disordered, and the decreases in elastic fibres and their fissures were moderate. In sharp contrast to group D. which showed marked calcium deposition, group D + Ela was found to have low calcium deposition. No macroscopic and histopathologic abnormalities were found in groups N and N + Ela. Elastase had an inhibitory effect on experimental atherosclerosis in the rat and also regulated the degradation and biosynthesis of elastin, which resulted in the regeneration of elastic fibres.

Animals↗

Diminished arterial elasticity in diabetes: association with fluorescent advanced glycosylation end products in collagen.

OBJECTIVE: Non-enzymatic glycosylation of proteins occurs in diabetes and advanced glycosylated end products can accumulate in long lived proteins such as vascular collagen and reduce the elasticity of vessel walls. To evaluate the potential association of advanced glycosylated end products in collagen with diminished arterial elasticity in diabetes, 14 diabetic and 14 age and sex matched non-diabetic patients with coronary artery disease were studied. METHODS: Arterial elasticity was assessed in terms of carotid to femoral pulse wave velocity and by measuring the change in ascending aortic diameter induced by pulse pressure. Collagen linked fluorescence, a measure of advanced glycosylated end products, was determined from tissue specimens of the skin, ascending aorta, and right atrial appendage taken during coronary bypass surgery. RESULTS: As a sign of diminished arterial elasticity, carotid to femoral pulse wave velocity was raised (p < 0.01) and change in ascending aortic diameter tended to be diminished (p = 0.09) in the diabetic patients. Collagen linked fluorescence was increased (p < 0.05) in the myocardium of the diabetic group, but the difference in skin and aorta was not significant. Collagen linked fluorescence between the aorta, skin, and myocardium correlated with each other (r = 0.64-0.77). Collagen linked fluorescence in the aorta and myocardium correlated with carotid to femoral pulse wave velocity (r = 0.63 and r = 0.67, respectively) in the diabetic group but not in the control group. CONCLUSIONS: These data suggest that non-enzymatic glycosylation of matrix proteins, and specifically collagen, may modify arterial elasticity in diabetic patients with coronary artery disease.

Adult↗

An evaluation of the transition temperature range of super-elastic orthodontic NiTi springs using differential scanning calorimetry.

Differential scanning calorimetry (DSC) was used to determine the transition temperature ranges (TTR) of four types of super-elastic orthodontic nickel-titanium coil springs (Sentalloy). A knowledge of the TTR provides information on the temperature at which a NiTi wire or spring can assume superelastic properties and when this quality disappears. The spring types in this study can be distinguished from each other by their characteristic TTR during cooling and heating. For each tested spring type a characteristic TTR during heating (austenite transformation) and cooling (martensite transformation) was evaluated. The hysteresis of the transition temperature, found between cooling and heating, was 3.4-5.2 K. Depending on the spring type the austenite transformation started (As) at 9.7-17.1 degrees C and finished (Af) at 29.2-37 degrees C. The martensite transformation starting temperature (Ms) was evaluated at 32.6-25.4 degrees C, while Mf (martensite transformation finishing temperature) was 12.7-6.5 degrees C. The results show that the springs become super-elastic when the temperature increases and As is reached. They undergo a loss of super-elastic properties and a rapid decrease in force delivery when they are cooled to Mf. For the tested springs, Mf and As were found to be below room temperature. Thus, at room temperature and some degrees lower, all the tested springs exert super-elastic properties. For orthodontic treatment this means the maintenance of super-elastic behaviour, even when mouth temperature decreases to about room temperature as can occur, for example, during meals.

Body Temperature↗

A sulphur matrix complex, elastic fibril composed of a fine core of amorphous elastin and microfibrils was largely accumulated in the aortic intima of aged rats.

We examined elastic fibrils in the aortic intima of aged rats with elastin staining, elastase digestion and X-ray microanalysis. The innermost elastic lamina, heavily stained by a brief treatment with azure II-toluidine blue without heating, was thin and fragmented, and an amorphous substance that stained weakly to moderately was accumulated in the thick subendothelial space of 26-28-month-old rat aortas. The substance was always present in the intimas; to a large extent in the aged rats but rarely in 5-month-old rats, and disappeared after digestion with elastase. The amorphous substance was identified as elastic fibrils approximately 0.1-0.2 microm in diameter under an electron microscope with tannic acid-uranyl acetate/lead citrate staining. Elastase digestion revealed that elastic fibrils were composed of a number of microfibrils, which were 10-12 nm in diameter, in and around a fine core of amorphous elastin. X-ray microanalysis revealed a clear peak of sulphur in the elastic fibrils.

Age Factors↗

The mechanism of interaction of sodium dodecyl sulfate with elastic fibers.

Sodium dodecyl sulfate (SDS), an anionic hydrophobic ligand, is known to alter the mechanical properties of elastic fibers. In order to analyze the mechanism of the alteration, two forms of fibrous elastins, "solid" and "powder" elastins, which consisted of fascicular elastic fibers and single or oligomeric elastic fibers, respectively, were prepared from bovine aorta, and the interactions of SDS with these elastins in the presence and absence of 0.15 M NaCl were studied. The solid elastin was able to retain 1.2- to 1.4-fold larger amounts of SDS than the powder elastin under both conditions, and both elastins retained 1.2-fold or larger amounts of SDS in the presence of NaCl than in its absence. Whereas both elastins released the retained SDS gradually on repeated washing with an SDS-free buffer, the release rates from the solid elastin, especially the rate in the presence of NaCl, were much smaller than those from the powder elastin, and the solid elastin retained approximately 40% of the bound SDS under conditions where the powder elastin lost most of its SDS. The SDS-binding capacities of both elastins were significantly lower than those of soluble kappa-elastin and serum albumin, which bound SDS homogeneously on the polypeptide chains. When the washed SDS-bound solid elastin was incubated with methylene blue and examined under a microscope, most of the methylene blue-SDS complex was located at the interfiber spaces of the elastic fibers. These results suggest that SDS alters the mechanical properties of elastic fibers by binding to the interfiber spaces and surfaces of the fibers rather than by binding to the internal polypeptide chains.

Animals↗