Journal articles: 'Distensibilità arteriosa'

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Tajaddini, Azita, Deborah L. Kilpatrick, Paul Schoenhagen, E. Murat Tuzcu, Michael Lieber, and D. Geoffrey Vince. "Impact of age and hyperglycemia on the mechanical behavior of intact human coronary arteries: an ex vivo intravascular ultrasound study." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 1 (January 2005): H250—H255. http://dx.doi.org/10.1152/ajpheart.00646.2004.

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Despite their advantages, percutaneous coronary interventional procedures are less effective in diabetic patients. Changes in the mechanical properties of vascular walls secondary to long-term hyperglycemia as well as other factors such as age may influence coronary distensibility. This investigation is aimed at deciphering the extent of these effects on distensibility of postmortem human coronary arteries in a controlled manner. Excised human left anterior descending (LAD) coronary arteries were obtained within 24 h postmortem. With the use of intravascular ultrasound, vascular deformation was analyzed at midregions of 51 moderate lesions. Intraluminal pressure was systematically altered using a computerized pressure pump system and monitored by a pressure-sensing guidewire. Distensibility, a normalized compliance term, was defined as the change in lumen area normalized by the initial reference area over a given pressure interval. With the use of multivariate analysis and repeated-measures ANOVA, coronary distensibility was independently influenced by hyperglycemia and age ( P < 0.05) through the entire pressure range. Within physiological pressure range, distensibility was significantly reduced with age in nonhyperglycemic coronary specimens (10.55 ± 4.41 vs. 6.99 ± 2.45, ×103 kPa−1, P = 0.01), whereas the hyperglycemic vessels were stiff even in the younger group (7.90 ± 5.82 vs. 7.20 ± 3.36, ×103 kPa−1, P = 0.79). Similar results were observed with stiffness index and elastic modulus of the arteries. Hyperglycemia and age independently influenced the distensibility of moderately atherosclerotic LAD coronary arteries. The stiffening with age was overshadowed in the hyperglycemic group by as-yet-undetermined factors.

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Bia, Daniel, Yanina Zócalo, Sandra Wray, and Edmundo I. Cabrera-Fischer. "Comparative in Vivo Analysis of the Role of the Adventitia and the Endothelium on Arterial Mechanical Function: Relevance for Aortic Counterpulsation." International Journal of Artificial Organs 40, no. 6 (May 24, 2017): 286–93. http://dx.doi.org/10.5301/ijao.5000585.

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Purpose The comparative effect of the intimal and adventitial layers on arterial biomechanics control, in basal and altered conditions, remains to be elucidated. This study aimed ( 1 ) to characterize the arterial conduit (CF) and buffering (distensibility) function of the iliac arteries in in vivo animals, in which the intimal and adventitial layers were removed; ( 2 ) to determine the effects of intra-aortic ballon pumping (IABP) on simultaneously de-adventitialized (DA) and de-endothelialized (DE) iliac arteries before and after induced heart failure. Methods Pressure and diameter signals were measured in the iliac arteries of sheep (n = 7) in which the adventitial and intima layer were removed. Intra-aortic balloon pump (IABP) assistance was used in a control state and after heart failure induction. Results Both DE and DA determined significant changes in arterial diameter, distensibility and CF. Changes were higher after DA than after DE in terms of distensibility and CF (p<0.05). DA followed by DE (DA + DE) showed significant increases in arterial diameter and CF, accompanied by a decrease in distensibility (p<0.05) with respect to intact arteries. Heart failure induction caused significant hemodynamic changes without modifying the already impaired local biomechanical parameters. Nonsignificant improvements in the biomechanical parameters of DA+ DE iliac arteries were observed during IABP before and after heart failure induction. Conclusions Biomechanical changes caused by DA of iliac arteries were more important than those observed after DE. The DA + DE arteries showed significant differences with respect to intact arteries and with DA or DE arteries. IABP-related effects on arterial mechanics were absent in DA+ DE arteries.

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Lee, Juhyun, Andrew Phan, and Jing Gao. "Multiparametric Ultrasound to Assess Adult Carotid Arteries." Journal for Vascular Ultrasound 44, no. 3 (June 1, 2020): 144–49. http://dx.doi.org/10.1177/1544316720927879.

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The aim of the study was to assess the value of multiparametric ultrasound in atherosclerotic cardiovascular disease risk screening of the carotid artery. We performed ultrasonography of carotid arteries in 96 adults in 3 age groups: senior (age ≥65 years, n = 44), middle age (age 45-64 years, n = 31), and young adults (age 20-44 years, n = 21). The senior group was then divided into subgroups: athletes (n = 21) and non-athletes (n = 23). Ultrasound parameters included carotid intima-media thickness, distensibility coefficient, and presence of plaque(s). Statistical analyses included one-way analysis of variance with post hoc to analyze the differences in ultrasound parameters among the age groups; unpaired t-test to examine differences between hypertensive and normotensive participants, between seniors with and without plaque(s), and between senior athletes and non-athletes; Pearson correlation coefficient to analyze correlations of ultrasound parameters to age and blood pressure; and intraclass correlation coefficient to test intra- and inter-observer reliability in performing multiparametric ultrasound. Carotid intima-media thickness and distensibility coefficient significantly differed among the 3 age groups and between athletes and non-athletes ( P < .001). Senior athletes had greater distensibility than non-athletes (all Ps < .05). Carotid intima-media thickness was increased and distensibility was reduced with age and hypertension. Age and blood pressure positively correlated with carotid intima-media thickness (Pearson correlation coefficient, r > .21) and negatively with distensibility coefficient (Pearson correlation coefficient, r < –.48). Inter- and intra-observer reliability in performing multiparametric ultrasound was good (intraclass correlation coefficient, r > .81). Multiparametric ultrasound is a useful tool to assess carotid artery function and morphology comprehensively.

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Cheung, Ning, A. Richey Sharrett, Ronald Klein, Michael H. Criqui, F. M. Amirul Islam, Katarzyna J. Macura, Mary Frances Cotch, Barbara E. K. Klein, and Tien Y. Wong. "Aortic Distensibility and Retinal Arteriolar Narrowing." Hypertension 50, no. 4 (October 2007): 617–22. http://dx.doi.org/10.1161/hypertensionaha.107.091926.

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Myers, Christopher W., William B. Farquhar, Daniel E. Forman, Todd D. Williams, Dustin L. Dierks, and J. Andrew Taylor. "Carotid distensibility characterized via the isometric exercise pressor response." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 6 (December 1, 2002): H2592—H2598. http://dx.doi.org/10.1152/ajpheart.00309.2002.

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Distensibility of the large elastic arteries is a key index for cardiovascular health. Distensibility, usually estimated from resting values in humans, is not a static characteristic but a negative curvilinear function of pressure. We hypothesized that differences in vascular function with gender and age may only be recognized if distensibility is quantified over a range of pressures. We used isometric handgrip exercise to induce progressive increases in pressures and carotid diameters, thereby enhancing the characterization of distensibility. In 30 volunteers, evenly distributed by gender and age across the third to fifth decades of life, we derived pulsatile distensibility slopes as a function of arterial pressure for a dynamic distensibility index and compared it with a traditional static index at a reference pressure of 95 mmHg. We also assessed intima-media thickness (IMT). We found that women had greater distensibility slopes within each decade, despite comparable IMT. Furthermore, declines in distensibility slope with increasing age were correlated to increased IMT. The static distensibility index failed to show gender-related differences in distensibility but did show age-related differences. Our results indicate that gender- and age-related differences can be manifest even in young, healthy adults and may only be identified with techniques that assess carotid distensibility across a range of pressures.

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De Meersman, Ronald E., Adrienne S. Zion, Elsa G. V. Giardina, Joseph P. Weir, James S. Lieberman, and John A. Downey. "Estrogen replacement, vascular distensibility, and blood pressures in postmenopausal women." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 5 (May 1, 1998): H1539—H1544. http://dx.doi.org/10.1152/ajpheart.1998.274.5.h1539.

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The pathogenesis of blood pressure (BP) rise in aging women remains unexplained, and one of the many incriminating factors may include abnormalities in arteriolar resistance vessels. The aim of this study was to determine the effects of unopposed estrogen on arteriolar distensibility, baroreceptor sensitivity (BRS), BP changes, and rate-pressure product (RPP). We tested the hypotheses that estrogen replacement therapy (ERT) enhances arteriolar distensibility and ameliorates BRS, which leads to decreases in BP and RPP. Postmenopausal women participated in a single-blind crossover study; the participants of this study, after baseline measurements, were randomly assigned to receive estrogen (ERT) or a drug-free treatment with a 6-wk washout period between treatments. The single-blind design was instituted because subjects become unblinded due to physiological changes (i.e., fluid shifts, weight gain, and secretory changes) associated with estrogen intake. However, investigators and technicians involved in data collection and analyses remained blind. After each treatment, subjects performed identical autonomic tests, during which electrocardiograms, beat-by-beat BPs, and respiration were recorded. The area under the dicrotic notch of the BP wave was used as an index of arteriolar distensibility. The magnitude of the reflex bradycardia after a precipitous rise in BP was used to determine BRS. Power spectral analysis of heart rate variability was used to assess autonomic activity. BPs were recorded from resistance vessels in the finger using a beat-by-beat photoplethysmographic device. RPP, a noninvasive marker of myocardial oxygen consumption, was calculated. Repeated-measures analyses of variance revealed a significantly enhanced arteriolar distensibility and BRS after ERT ( P < 0.05). A trend of a lower sympathovagal balance at rest was observed after ERT; however, this trend did not reach statistical significance ( P = 0.061) compared with the other treatments. The above autonomic changes produced significantly lower systolic and diastolic BP changes and RPPs ( P < 0.05) at rest and during isometric exercise. We conclude that short-term unopposed ERT favorably enhances arteriolar distensibility, BRS, and hemodynamic parameters in postmenopausal women. These findings have clinical implications in the goals for treating cardiovascular risk factors in aging women.

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Zhang, Yunlong, and Sandra T. Davidge. "Estrogen replacement increases coronary artery distensibility in ovariectomized rats." Canadian Journal of Physiology and Pharmacology 77, no. 1 (January 1, 1999): 75–78. http://dx.doi.org/10.1139/y98-145.

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The effect of estrogen on the passive characteristics of arteries is not known. We hypothesized that estrogen would increase arterial distensibility as part of its protective effect on the vasculature. Female Sprague-Dawley rats were ovariectomized at 11 weeks of age. One group received a placebo (n = 6), while two other groups (n = 5 each) of rats received a 17β-estradiol pellet (0.15 mg or 0.5 mg with 60-day release). After 4 weeks of estrogen replacement, coronary and mesenteric arteries (<200 µm diameter) were dissected and mounted on a dual-chamber arteriograph. Lumen diameter and wall thickness were measured in pressurized arteries. The relative changes in diameter (distensibility) as well as wall thickness per unit change in pressure were significantly increased (p < 0.05) in the coronary arteries of the 0.5 mg estradiol replaced rats compared with the ovariectomized control animals and the 0.15 mg estradiol replaced rats. Surprisingly, in the mesenteric arteries from the same animals, there was no difference in distensibility or pressure - wall thickness among the groups. This study provides experimental data of a novel hypothesis that estrogen may afford part of its protection through vascular remodeling of the coronary circulation.Key words: vasculature, remodeling, cardiovascular disease.

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Baumbach, G. L., J. E. Siems, F. M. Faraci, and D. D. Heistad. "Mechanics and composition of arterioles in brain stem and cerebrum." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 2 (February 1, 1989): H493—H501. http://dx.doi.org/10.1152/ajpheart.1989.256.2.h493.

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The goal of this study was to compare mechanics and composition of arterioles in brain stem and cerebrum. We calculated stress and strain of pial arterioles in anesthetized rats from measurements of pial arteriolar pressure (servo-null), diameter, and cross-sectional area of the vessel wall. Composition of pial arterioles was quantitated using point-counting stereology. Before deactivation of smooth muscle with ethylenediaminetetraacetic acid (EDTA), pial arteriolar pressure and diameter were 28 and 30% greater (P less than 0.05) in brain stem than cerebrum. After EDTA, diameter of arterioles was similar in brain stem and cerebrum. Cross-sectional area of the arteriolar wall was 32% greater (P less than 0.05) in brain stem than cerebrum. Stress-strain curves indicated that distensibility of pial arterioles is greater in brain stem than cerebrum. The proportion of nondistensible (collagen and basement membrane) to distensible (elastin, smooth muscle, and endothelium) components was 20% less (P less than 0.05) in brain stem than cerebral arterioles. We conclude that 1) cross-sectional area of the vessel wall in arterioles of comparable size is greater in brain stem than cerebrum, 2) distensibility of arterioles is greater in brain stem than cerebrum, despite greater cross-sectional area of the arteriolar wall in brain stem, and 3) the proportion of elastic components is greater in brain stem than cerebral arterioles, which may contribute to greater arteriolar distensibility in brain stem.

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Hillier, S. C., P. S. Godbey, C. C. Hanger, J. A. Graham, R. G. Presson, O. Okada, J. H. Linehan, C. A. Dawson, and W. W. Wagner. "Direct measurement of pulmonary microvascular distensibility." Journal of Applied Physiology 75, no. 5 (November 1, 1993): 2106–11. http://dx.doi.org/10.1152/jappl.1993.75.5.2106.

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Pulmonary vascular distensibility has an important influence on pulmonary hemodynamics. Although many measurements of distensibility have been made on large pulmonary vessels, there is less information on microvascular distensibility. We have measured the distensibility of the smallest (< 70-microns-diam) precapillary arterioles and postcapillary venules. Isolated dog lobes, at 2.5 cmH2O transpulmonary pressure, were perfused at low flows, which caused the arteriovenous pressure gradient to be very small and thereby permitted accurate estimation of microvascular pressure. As microvascular pressure was systematically varied between 0 and 30 mmHg, subpleural microvascular diameters were determined from computer-enhanced images obtained by videomicroscopy. Arteriolar and venular distensibilities were not different from each other. The microvascular pressure-diameter relationship was alinear with distensibility coefficients of 1–3% mmHg-1, values that are of the same order of magnitude as previously measured distensibilities of 100- to 1,000-microns-diam canine pulmonary vessels.

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Hoeks, A. P. G., P. J. Brands, F. A. M. Smeets, and R. S. Reneman. "Assessment of the distensibility of superficial arteries." Ultrasound in Medicine & Biology 16, no. 2 (January 1990): 121–28. http://dx.doi.org/10.1016/0301-5629(90)90139-4.

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SØRENSEN, V. B., P. ROSSING, L. TARNOW, H. H. PARVING, T. NØRGAARD, and J. KASTRUP. "Effects of nisoldipine and lisinopril on microvascular dysfunction in hypertensive Type I diabetes patients with nephropathy." Clinical Science 95, no. 6 (December 1, 1998): 709–17. http://dx.doi.org/10.1042/cs0950709.

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1. Our objective was to compare the effect of a long-acting calcium antagonist (nisoldipine) compared with an angiotensin-converting enzyme inhibitor (lisinopril) on the non-neurogenic regulation of the microvascular blood flow in hypertensive Type I diabetes patients with diabetic nephropathy. 2. We performed a 1-year double-blind, double-dummy randomized controlled study comparing nisoldipine (20–40 mg once daily) with lisinopril (10–20 mg once daily) in 48 hypertensive Type I diabetes patients with diabetic nephropathy. For comparison, 22 age-matched normotensive healthy control subjects were included. Measurements were performed at baseline and after 1 year of antihypertensive treatment. The minimal vascular resistance and distensibility (stiffness) of resistance vessels in skin and skeletal muscle were measured using the local isotope washout method. 3. Mean arterial pressure was reduced to the same extent in both groups: nisoldipine, 113±2.1 to 105±1.6 mmHg (P< 0.001); lisinopril, 110±2.7 to 101±2.1 mmHg (P< 0.002) (controls, 88±2.2 mmHg; P< 0.0001 compared with diabetic patients). Nisoldipine improved the skin vascular distensibility from 28±3.3 to 43±3.8% (P< 0.005) and decreased skin minimal vascular resistance from 16.9±1.0 to 13.6±0.8 mmHg·ml-1·min·100 g (P< 0.02). Lisinopril had no significant effect on skin vascular distensibility (40±4.0% and 41±4.4%), but minimal vascular resistance tended to diminish (18.1±0.9 to 15.8±1.3 mmHg·ml-1·min·100 g (P =0.09). Nisoldipine significantly increased the skin distensibility (P = 0.05) after 1 year of antihypertensive treatment compared with lisinopril. 4. The control group had a skin vascular distensibility of 54±3.2% and a minimal vascular resistance of 10.8±0.7 mmHg·ml-1·min·100 g, both significantly different from the values in the diabetic groups (P< 0.0001 for all). Skeletal muscle vascular distensibility was unaltered after 1 year of treatment with both nisoldipine (22±3.3% and 19±2.7%) and lisinopril (19±2.1% and 24±2.5%), but was reduced compared with a control value of 43±3.7% (P< 0.0001 for diabetes patients versus controls). However, neither nisoldipine nor lisinopril had any effect on the increased minimal vascular resistance or the reduced skeletal muscle distensibility. 5. Enhanced thickening of the basement membranes of the terminal arteriolar wall was found in skin biopsy specimens in 91% of diabetic patients and 38% only in control subjects (P< 0.000001 both before and after treatment for diabetic patients versus controls). There was no significant effect of antihypertensive treatment on arteriolar hyalinosis. 6. The reduction in systemic blood pressure was identical during 1 year of treatment with nisoldipine or lisinopril. The abnormal arteriolar stiffness was more pronounced in the group treated with nisoldipine than with lisinopril and only nisoldipine compared with lisinopril improved the abnormal arteriolar stiffness and minimal vascular resistance in the skin. This suggests that nisoldipine can reverse the peripheral skin perfusion and thereby improve the local protection against development of ischaemic skin lesions in Type I diabetes patients with clinical diabetic nephropathy.

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Salvi, Paolo, Filippo Valbusa, Anna Kearney-Schwartz, Carlos Labat, Andrea Grillo, Gianfranco Parati, and Athanase Benetos. "Non-Invasive Assessment of Arterial Stiffness: Pulse Wave Velocity, Pulse Wave Analysis and Carotid Cross-Sectional Distensibility: Comparison between Methods." Journal of Clinical Medicine 11, no. 8 (April 15, 2022): 2225. http://dx.doi.org/10.3390/jcm11082225.

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Background: The stiffening of large elastic arteries is currently estimated in research and clinical practice by propagative and non-propagative models, as well as parameters derived from aortic pulse waveform analysis. Methods: Common carotid compliance and distensibility were measured by simultaneously recording the diameter and pressure changes during the cardiac cycle. The aortic and upper arm arterial distensibility was estimated by measuring carotid–femoral and carotid–radial pulse wave velocity (PWV), respectively. The augmentation index and blood pressure amplification were derived from the analysis of central pulse waveforms, recorded by applanation tonometry directly from the common carotid artery. Results: 75 volunteers were enrolled in this study (50 females, average age 53.5 years). A significant inverse correlation was found between carotid distensibility and carotid–femoral PWV (r = −0.75; p < 0.001), augmentation index (r = −0.63; p < 0.001) and central pulse pressure (r = −0.59; p < 0.001). A strong correlation was found also between the total slope of the diameter/pressure rate carotid curves and aortic distensibility, quantified from the inverse of the square of carotid–femoral PWV (r = 0.67). No correlation was found between carotid distensibility and carotid–radial PWV. Conclusions: This study showed a close correlation between carotid–femoral PWV, evaluating aortic stiffness by using the propagative method, and local carotid cross-sectional distensibility.

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Carretta, R., F. Vran, M. Bardelli, B. Fabris, F. Fischetti, G. Bulli, and L. Campanacci. "Large arteries distensibility after therapy with calcium antagonists." Pharmacological Research 22 (September 1990): 94. http://dx.doi.org/10.1016/s1043-6618(09)80141-2.

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al-Tinawi, A., J. A. Madden, C. A. Dawson, J. H. Linehan, D. R. Harder, and D. A. Rickaby. "Distensibility of small arteries of the dog lung." Journal of Applied Physiology 71, no. 5 (November 1, 1991): 1714–22. http://dx.doi.org/10.1152/jappl.1991.71.5.1714.

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To obtain in situ measurements of the distensibility of small (100- to 1,000-microns-diam) pulmonary arterial vessels of the dog lung, X-ray angiograms were obtained from isolated lung lobes with the vascular pressure adjusted to various levels. The in situ diameter-pressure relationships were compared with the diameter-pressure relationships for small arteries that were dissected free from the lungs and cannulated with small glass pipettes for the measurement of diameter and transmural pressure. The diameter-vascular or diameter-transmural pressure curves from both in situ and cannulated vessels were sufficiently linear in the pressure range studied (0–30 Torr) that they could be characterized by linear regression to obtain estimates of D0, the diameter at zero vascular pressure, and beta, the change in diameter (micron) per Torr change in pressure. The vessel distensibility coefficient (alpha) was defined as alpha = beta/D0. The mean values of alpha were approximately 2.0 +/- 0.8%/Torr (SD) for the in situ vessels and 1.7 +/- 0.6%/Torr for the cannulated vessels, with no statistically significant difference between the two methods. The influence of vasoconstriction elicited by serotonin was evaluated in the in situ vessels. Serotonin-induced vasoconstriction caused a decrease in D0 and little change in alpha.

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Douglas, Gillian, M. Natalia Cruz, Lucilla Poston, Jan-Åke Gustafsson, and Karolina Kublickiene. "Functional characterization and sex differences in small mesenteric arteries of the estrogen receptor-β knockout mouse." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 1 (January 2008): R112—R120. http://dx.doi.org/10.1152/ajpregu.00421.2007.

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The role of the estrogen receptor (ER) subtypes in the modulation of vascular function is poorly understood. The aim of this study was to characterize ex vivo the functional properties of small arteries and their response to estrogens in the mesenteric circulation of female and male ER-β knockout mice (β-ERKO) and their wild-type (WT) littermates. Responses to changes in intraluminal flow and pressure were obtained before and after incubation with 17β-estradiol or ER-α agonist propyl-pyrazole-triol (3 h; 10 nM). Cumulative concentration-response curves to acetylcholine, norepinephrine, and passive distensibility were compared with respect to sex and genotype. The collagen and elastin content within the vascular wall and ER expression were also determined. Endothelial morphology was visualized by scanning electron microscopy. 17β-Estradiol and propyl-pyrazole-triol-treated arteries from female β-ERKO and WT mice showed enhanced flow-mediated dilation, but this was not evident in males. Distensibility was decreased in arteries from β-ERKO females. Sex differences in myogenic tone were observed in 17β-estradiol-treated arteries, but were similar between β-ERKO and WT mice. Acetylcholine- and norepinephrine-induced responses were similar between groups and sexes. ER-α was similarly expressed in the endothelium and media of arteries from all groups studied, as well as ER-β in WT animals. Endothelial morphology was similar in arteries from animals of both sexes and genotype; however, arterial elastin content was decreased, and collagen content was increased in β-ERKO male compared with WT male and with β-ERKO female. We suggest that ERs play a sex-specific role in estrogen-mediated flow responses and distensibility, and that deletion of ER-β affects artery structure but only in male animals. Further studies in β-ERKO mice with established hypertension and in α-ERKO mice are warranted.

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Frisbee, Jefferson C. "Impaired skeletal muscle perfusion in obese Zucker rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 285, no. 5 (November 2003): R1124—R1134. http://dx.doi.org/10.1152/ajpregu.00239.2003.

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Skeletal muscle arterioles from obese Zucker rats (OZR) exhibit oxidant stress-based alterations in reactivity, enhanced α-adrenergic constriction, and reduced distensibility vs. microvessels of lean Zucker rats (LZR). The present study determined the impact of these alterations for perfusion and performance of in situ skeletal muscle during periods of elevated metabolic demand. During bouts of isometric tetanic contractions, fatigue of in situ gastrocnemius muscle of OZR was increased vs. LZR; this was associated with impaired active hyperemia. In OZR, vasoactive responses of skeletal muscle arterioles from the contralateral gracilis muscle were impaired, due in part to elevated oxidant tone; reactivity was improved after treatment with polyethylene glycol-superoxide dismutase (PEGSOD). Arterioles of OZR also exhibited increased α-adrenergic sensitivity, which was abolished by treatment with phentolamine (10-5 M). Intravenous infusion of phentolamine (10 mg/kg) or PEG-SOD (2,000 U/kg) in OZR altered neither fatigue rates nor active hyperemia from untreated levels; however, combined infusion improved performance and hyperemia, although not to levels in LZR. Microvessel density in the contralateral gastrocnemius muscle, determined via histological analyses, was reduced by ∼25% in OZR vs. LZR, while individual arterioles from the contralateral gracilis muscle demonstrated reduced distensibility. These data suggest that altered arteriolar reactivity contributes to reduced muscle performance and active hyperemia in OZR. Further, despite pharmacological improvements in arteriolar reactivity, reduced skeletal muscle microvessel density and arteriolar distensibility also contribute substantially to reduced active hyperemia and potentially to impaired muscle performance.

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Madden, J. A., P. A. Keller, R. M. Effros, C. Seavitte, J. S. Choy, and A. D. Hacker. "Responses to pressure and vasoactive agents by isolated pulmonary arteries from monocrotaline-treated rats." Journal of Applied Physiology 76, no. 4 (April 1, 1994): 1589–93. http://dx.doi.org/10.1152/jappl.1994.76.4.1589.

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Intralobar and side branch pulmonary arteries removed from rats 7, 14, and 21 days after injection with monocrotaline (MCT) were cannulated and pressurized, and their responses to potassium chloride, norepinephrine, acetylcholine, and angiotensin II were measured. Static pressure-diameter curves were also performed, and arterial distensibility was calculated. Arteries from all three MCT-treated groups showed reduced responses to potassium chloride and angiotensin II compared with control arteries (P < 0.05). The norepinephrine response was significantly reduced in arteries from the 14- and 21-day groups (P < 0.05). Dilations in response to acetylcholine were similar in arteries from the control and 7-day groups but were reduced compared with those in control vessels from the 14- and 21-day groups (P < 0.05). Compared with control values, the slopes of the pressure-diameter curves and the arterial distensibility decreased significantly with time after MCT treatment (P < 0.05). Values for arterial distensibilities obtained in the isolated pulmonary arteries support the theory that structural changes that occur as a result of MCT administration contribute to vessel stiffness. The acetylcholine-induced dilation of vessels from MCT-treated rats indicates that endothelium-derived factors are still produced, but diminished vasodilation coupled with decreased distensibilities after MCT suggest that abnormal vascular remodeling rather than a change in agonist sensitivity may be responsible for the reduced responsiveness seen in these arteries.

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Haworth, S. T., J. H. Linehan, T. A. Bronikowski, and C. A. Dawson. "A hemodynamic model representation of the dog lung." Journal of Applied Physiology 70, no. 1 (January 1, 1991): 15–26. http://dx.doi.org/10.1152/jappl.1991.70.1.15.

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The published morphometric data from human, cat, and dog lungs suggest that the power-law relationships between the numbers (Na and Nv) and diameters (Da and Dv) of arteries and veins and between the lengths (La and Lv) and diameters of the arteries and veins could be used as scaling rules for assigning dimensions and numbers to the intrapulmonary vessels of the arterial and venous trees of the dog lung. These rules, along with the dimensions of the extrapulmonary arteries and capillary sheet and the distensibility coefficients of the vessels obtained from the literature, were used to construct a steady-state hemodynamic model of the dog lung vascular bed. The model can be characterized approximately by 15 orders of arteries with Na approximately 2.07 Da-2.58 and 13 orders of veins with Nv approximately 2.53 Dv-2.61. For the intrapulmonary vessels (orders 1–12), La approximately 4.85 Da1.01, and Lv approximately 6.02 Da1.07. The average ratio of the numbers of vessels in consecutive orders is approximately 3.2 for the arteries and veins. These arterial and venous trees are connected by the capillary sheet with an undistended thickness of approximately 3.5 microns and an area of 33 m2. The average distensibility (% increase in diameter over the undistended diameter/Torr increase in transmural pressure) for the model arteries and veins is approximately 2.4%/Torr, and the distensibility of the capillary sheet (% increase in thickness over the undistended thickness/Torr increase in transmural pressure) is approximately 3.6%/Torr. The calculated arterial-capillary-venous volumes and compliances of the model agree well with experimental estimates of these variables in dogs. In addition, the model appears consistent with certain aspects of the pressure-flow relationships measured in dog lungs. The model appears to be a useful summary of some of the available data on pulmonary morphometry and vessel properties. It is anticipated that the model will provide the basis for dynamic modeling of the dog lung in the future.

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Zulliger, Martin A., Naomi T. M. R. Kwak, Theodora Tsapikouni, and Nikos Stergiopulos. "Effects of longitudinal stretch on VSM tone and distensibility of muscular conduit arteries." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 6 (December 1, 2002): H2599—H2605. http://dx.doi.org/10.1152/ajpheart.00298.2002.

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With progressing age, large arteries diminish their longitudinal stretch, which in extreme cases results in tortuosity. Increased age is also associated with loss of vessel distensibility. We measured pressure-diameter curves from muscular porcine carotid arteries ex vivo at different longitudinal stretch ratios (λ z = 1.4 and 1.8) and under different vascular smooth muscle (VSM) conditions (fully relaxed, normal VSM tone, and maximally contracted). Distensibility was found to be halved by decreasing longitudinal stretch from λ z = 1.8 to 1.4 at physiological pressures. This counterintuitive observation is possible because highly nonlinear elastic modulus of the artery and anisotropic properties. Furthermore, a significantly larger basal VSM contraction was observed at λ z = 1.8 than 1.4, although this was clearly not related to a myogenic response during inflation. This dependence of VSM tone to longitudinal stretch may have possible implications on the functional characteristics of the arterial wall.

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Tozzi, C. A., D. L. Christiansen, G. J. Poiani, and D. J. Riley. "Excess collagen in hypertensive pulmonary arteries decreases vascular distensibility." American Journal of Respiratory and Critical Care Medicine 149, no. 5 (May 1994): 1317–26. http://dx.doi.org/10.1164/ajrccm.149.5.8173773.

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Demer, Linda L., Mehrdad Ariani, and Robert J. Siegel. "High intensity ultrasound increases distensibility of calcific atherosclerotic arteries." Journal of the American College of Cardiology 18, no. 5 (November 1991): 1259–62. http://dx.doi.org/10.1016/0735-1097(91)90544-j.

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Berthon, Nathalie, Pascal Laurant, Daniel Hayoz, Dominique Fellmann, Hans R. Brunner, and Alain Berthelot. "Magnesium supplementation and deoxycorticosterone acetate salt hypertension: effect on arterial mechanical properties and on activity of endothelin-1." Canadian Journal of Physiology and Pharmacology 80, no. 6 (June 1, 2002): 553–61. http://dx.doi.org/10.1139/y02-082.

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The aim of this study was to show whether the decrease in blood pressure induced by Mg supplementation in deoxycorticosterone acetate salt (DOCAsalt) hypertensive rats is associated with mechanical modifications of blood vessels and (or) changes in tissular production and (or) vasoconstrictor activity to endothelin-1. DOCAsalt treatment increased blood pressure, media thickness, cross-sectional area, and lumen diameter of carotid arteries. Distensibility and incremental elastic modulus versus stress were not altered in carotid arteries, suggesting that the DOCAsalt vessel wall adapts structurally to preserve its blood pressure buffering capacity. Magnesium supplementation attenuated DOCAsalt hypertension. In comparison with normotensive rats, systolic, mean, and pulse pressures were higher whereas diastolic pressure was not different in Mg-supplemented DOCA-salt rats. Magnesium supplementation did not significantly modify the elastic parameters of carotid arteries. In resistance mesenteric arteries, DOCAsalt hypertension induces an inward hypertrophic remodeling. Magnesium supplementation attenuates wall hypertrophy and increases lumen diameter to the normotensive diameter, suggesting a decrease in peripheral resistance. Magnesium supplementation normalizes the altered vasoconstrictor activity of endothelin-1 in mesenteric arteries and attenuates endothelin-1 overproduction in kidney, left ventricle, and aorta of DOCA-salt rats. These findings suggest that Mg supplementation prevents blood pressure elevation by attenuating peripheral resistance and by decreasing hypertrophic effect of endothelin-1 via inhibition of endothelin-1 production.Key words: hypertension, resistance, distensibility, blood vessels, magnesium.

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Genkel, Vadim V., Alexey O. Salashenko, Tatyana N. Shamaeva, Veronika A. Sumerkina, and Igor I. Shaposhnik. "Association between Carotid Wall Shear Rate and Arterial Stiffness in Patients with Hypertension and Atherosclerosis of Peripheral Arteries." International Journal of Vascular Medicine 2018 (August 1, 2018): 1–8. http://dx.doi.org/10.1155/2018/6486234.

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Aim. To evaluate carotid wall shear rate (WSR) in association with local and regional vascular stiffness in patients with hypertension (HTN) and atherosclerosis of peripheral arteries and to study the pattern of change of WSR in patients with HTN with increasing severity of peripheral artery atherosclerosis. Materials and Methods. Study involved 133 patients with HTN, 65 men and 48 women, aged in average 57.9±10.8 years. All patients were divided into four groups in accordance with ultrasound morphologic classification of vessel wall. Duplex scanning of carotid and lower limb arteries was performed. Carotid-femoral (cfPWV) and carotid-radial (crPWV) pulse wave velocity (PWV) were measured. Local carotid stiffness was evaluated by carotid ultrasound. Results. WSR of patients with plaques without and with hemodynamic disturbance was 416±128 s−1 and 405±117 s−1, respectively, which was significantly less than the WSR in patients with intact peripheral arteries – 546±112 s−1. Decreased carotid WSR was associated with increased crPVW, cfPWV, Peterson’s elastic modulus, decreased distensibility, and distensibility coefficient. Conclusion. In patients with HTN and atherosclerotic lesions of peripheral arteries, it is registered that the carotid WSR decreased with increasing severity of atherosclerosis. Decreased carotid WSR is associated with increased local carotid stiffness, regional vascular stiffness of muscular, and elastic vessels.

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Frisbee, Jefferson C. "Reduced nitric oxide bioavailability contributes to skeletal muscle microvessel rarefaction in the metabolic syndrome." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 2 (August 2005): R307—R316. http://dx.doi.org/10.1152/ajpregu.00114.2005.

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This study tested the hypothesis that chronically elevated oxidant stress contributes to impaired active hyperemia in skeletal muscle of obese Zucker rats (OZR) vs. lean Zucker rats (LZR) through progressive deteriorations in microvascular structure. Twelve-week-old LZR and OZR were given 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (tempol) in the drinking water for ∼4 wk. Subsequently, perfusion of in situ gastrocnemius muscle was determined during incremental elevations in metabolic demand, while a contralateral skeletal muscle arteriole and the gastrocnemius muscle was removed to determine dilator reactivity, vessel wall mechanics, and microvessel density. Under control conditions, active hyperemia was impaired at all levels of metabolic demand in OZR, and this was correlated with a reduced microvessel density, increased arteriolar stiffness, and impaired dilator reactivity. Chronic tempol ingestion improved perfusion during moderate to high metabolic demand only and was associated with improved arteriolar reactivity and microvessel density; passive vessel mechanics were unaltered. Combined antioxidant therapy and nitric oxide synthase inhibition in OZR prevented much of the restored perfusion and microvessel density. In LZR, treatment with Nω-nitro-l-arginine methyl ester (l-NAME) hydrochloride and hydralazine (to prevent hypertension) impaired active hyperemia, dilator reactivity, and microvessel density, although arteriolar distensibility was not altered. These results suggest that with the development of the metabolic syndrome, chronic reductions in nitric oxide bioavailability, in part via the scavenging actions of oxidative free radicals, contribute to a loss of skeletal muscle microvessels, leading to impaired muscle perfusion with elevated metabolic demand.

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Osol, George, Carolyn Barron, and Maurizio Mandalà. "Uterine distension differentially affects remodelling and distensibility of the uterine vasculature in non-pregnant rats." Reproduction, Fertility and Development 24, no. 6 (2012): 835. http://dx.doi.org/10.1071/rd11208.

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During pregnancy the mammalian uterine circulation undergoes significant expansive remodelling necessary for normal pregnancy outcome. The underlying mechanisms are poorly defined. The goal of this study was to test the hypothesis that myometrial stretch actively stimulates uterine vascular remodelling by developing a new surgical approach to induce unilateral uterine distension in non-pregnant rats. Three weeks after surgery, which consisted of an infusion of medical-grade silicone into the uterine lumen, main and mesometrial uterine artery and vein length, diameter and distensibility were recorded. Radial artery diameter, distensibility and vascular smooth muscle mitotic rate (Ki67 staining) were also measured. Unilateral uterine distension resulted in significant increases in the length of main uterine artery and vein and mesometrial segments but had no effect on vessel diameter or distensibility. In contrast, there were significant increases in the diameter of the radial arteries associated with the distended uterus. These changes were accompanied by reduced arterial distensibility and increased vascular muscle hyperplasia. In summary, this is the first report to show that myometrial stretch is a sufficient stimulus to induce significant remodelling of uterine vessels in non-pregnant rats. Moreover, the results indicate differential regulation of these growth processes as a function of vessel size and type.

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Roy, Sylvain, Paolo Silacci, and Nikolaos Stergiopulos. "Biomechanical proprieties of decellularized porcine common carotid arteries." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 4 (October 2005): H1567—H1576. http://dx.doi.org/10.1152/ajpheart.00564.2004.

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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.

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Hajdu, M. A., and G. L. Baumbach. "Mechanics of large and small cerebral arteries in chronic hypertension." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 3 (March 1, 1994): H1027—H1033. http://dx.doi.org/10.1152/ajpheart.1994.266.3.h1027.

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The goal of this study was to investigate factors that contribute to reductions in internal diameter of large and small cerebral arteries during chronic hypertension. We measured diameter of second- and third-order branches of the posterior cerebral artery in vitro during maximal dilation with EDTA in 6-mo-old stroke-prone spontaneously hypertensive rats (SHRSP, n = 7) and Wistar-Kyoto rats (WKY, n = 7). Cross-sectional area of the vessel wall, measured histologically, was not significantly different at 70 mmHg in SHRSP and WKY in large or small branches of posterior cerebral artery. In large branches of posterior cerebral artery, external and internal diameters were significantly less at 70 mmHg in SHRSP than in WKY, whereas external and internal diameters converged at 0 mmHg in the two groups of rats. In small branches, on the other hand, external and internal diameters were significantly less at all levels of intravascular pressure in SHRSP than in WKY. The stress-strain relation in posterior cerebral artery of SHRSP was shifted to the left in large branches and to the right in small branches, which indicates that distensibility was reduced in large cerebral arteries of SHRSP and increased in small cerebral arteries. These findings suggest that different mechanisms are responsible for impairment of maximal dilator capacity in large and small cerebral arteries of SHRSP: reduced distensibility in large arteries and remodeling with reduced external diameter in small arteries. Furthermore the findings provide additional support for the concept that hypertrophy may not be a primary factor in impaired maximal dilation.

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Wroblewski, H., T. Norgaard, S. Haunso, and J. Kastrup. "Microvascular distensibility in two different vascular beds in idiopathic dilated cardiomyopathy." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 6 (December 1, 1995): H1973—H1980. http://dx.doi.org/10.1152/ajpheart.1995.269.6.h1973.

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The local isotope-washout technique allows discrimination between blood flow in skin and muscle. Arteriolar constriction, mediated by the sympathetic nervous system, is abolished in a papaverine-histamine-relaxed vascular bed. Microvascular distensibility of relaxed resistance vessels was measured in skeletal muscle and skin of the lower limb in patients with congestive heart failure (CHF) secondary to idiopathic dilated cardiomyopathy and in healthy subjects. Vascular transmural pressure was elevated 40 mmHg by head-up tilt and caused muscle blood flow to increase by 11 +/- 9% in 20 CHF patients compared with 44 +/- 20% in 11 control subjects (P < 0.0003). Also the increase in skin blood flow was significantly reduced: 31 +/- 18% in 42 CHF patients compared with 62 +/- 29% in 25 control subjects (P < 0.001). Regression analysis demonstrated a significant association between microvascular distensibility in skin and skeletal muscle tissue (P = 0.003, r = 0.51, n = 31). Structure of terminal arterioles was determined in skin biopsies, and structural microangiopathy was found in 32 of 42 CHF patients. Multiple regression analysis demonstrated the degree of microangiopathy to be the only parameter significantly associated with microvascular distensibility (P = 0.005, r = 0.42). (There was no association to NY Heart Association functional class, left ventricular ejection fraction, duration of CHF, age of subject, or mean arterial blood pressure.) We conclude that patients with idiopathic dilated cardiomyopathy have similar decreased microvascular distensibility in skeletal muscle and skin. Furthermore, structural alterations in terminal arterioles seem to be associated with decreased distensibility and increased stiffness of the cutaneous microvascular bed.

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Flahault, Adrien, Rafael Oliveira Fernandes, Julie De Meulemeester, Daniela Ravizzoni Dartora, Anik Cloutier, Geneviève Gyger, Ramy El-Jalbout, Jean-Luc Bigras, Thuy Mai Luu, and Anne Monique Nuyt. "Arterial Structure and Stiffness Are Altered in Young Adults Born Preterm." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 10 (October 2020): 2548–56. http://dx.doi.org/10.1161/atvbaha.120.315099.

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Objective: Preterm birth has been associated with changes in arterial structure and function. Association with complications occurring during the neonatal period, including bronchopulmonary dysplasia, on vascular outcomes in adulthood is unknown. Approach and Results: We evaluated a cohort of 86 adults born preterm (below 30 weeks of gestation), compared to 85 adults born term, at a mean age of 23 years. We performed ultrasonographic assessment of the dimensions of the ascending aorta, carotid and brachial arteries, and estimated flow-mediated dilation, carotid-femoral pulse wave velocity, augmentation index corrected for heart rate, and carotid intima-media thickness. All analyses were performed with and without adjustment for potential confounding variables, including height, sex, and body mass index. Ascending aorta diameter in diastole was smaller in the preterm group, but carotid and brachial arteries were similar. Carotid and brachial strain, a marker of arterial distensibility, was smaller in the preterm group, while carotid-femoral pulse wave velocity, was similar between groups, indicating similar aortic stiffness. Carotid intima-media thickness, endothelial function flow-mediated dilation, blood nitrite, and nitrate levels were similar between groups. Individuals with bronchopulmonary dysplasia had lower brachial artery strain suggesting long-term association of this neonatal complication with vascular structure. Diastolic blood pressure was higher in the preterm group and was associated with decreased brachial and carotid distensibility. Conclusions: Young adults born preterm display alterations in arterial distensibility that are associated with a history of bronchopulmonary dysplasia.

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Catalano, Maria, Giovanni Scandale, Tao Jun, Marzio Minola, Martino Recchia, and Massimo Annoni. "Radial Artery Compliance in Patients with Peripheral Vascular Disease." Vascular Medicine 2, no. 1 (February 1997): 8–12. http://dx.doi.org/10.1177/1358863x9700200102.

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Compliance in largely central arteries of patients with peripheral vascular disease (PVD) has been reported to be reduced. However, the arterial tree is an inhomogeneous system, and there remains uncertainty about whether the peripheral arteries (e.g. the medium-sized muscular radial artery) undergo a similar change to the central arteries. The aim of this study was to investigate the radial artery elasticity in 19 patients with PVD compared with 18 normal subjects of comparable age and sex. Using a noninvasive high-resolution echo-tracking device coupled to a photoplethysmograph (Finapres system) allowing simultaneous arterial diameter and finger blood pressure monitoring, we measured the radial artery compliance by determining the diameter–pressure, compliance–pressure and distensibility–pressure curves. The results showed that the diameter of the radial artery was similar in the two groups, but that the compliance and distensibility were not further reduced in patients with PVD than in the normal controls at 100 mmHg and for a common blood pressure range. The present studies demonstrate that in patients with PVD the radial arterial compliance is not reduced, which indicates that the change in arterial elasticity is not identical. The potential mechanisms involved in this change in radial artery compliance are discussed.

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Simon, Geza, Marta Jaeckel, and Gyorgy Illyes. "Altered structure and distensibility of arteries in salt-fed rats." Journal of Hypertension 21, no. 1 (January 2003): 137–43. http://dx.doi.org/10.1097/00004872-200301000-00023.

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Salvi, Paolo, and Gianfranco Parati. "Augmentation index as a specific marker of large arteries distensibility." Journal of Hypertension 30, no. 12 (December 2012): 2276–78. http://dx.doi.org/10.1097/hjh.0b013e32835aa0df.

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Laurant, Pascal, Mark Adrian, and Alain Berthelot. "Effect of age on mechanical properties of rat mesenteric small arteries." Canadian Journal of Physiology and Pharmacology 82, no. 4 (April 1, 2004): 269–75. http://dx.doi.org/10.1139/y04-026.

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With aging, large arteries become stiffer and systolic blood pressure consequently increases. Less is known, however, about the age-related change in mechanics of small resistance arteries. The aim of this study was to determine whether aging plays a role in the stiffening of the small mesenteric arteries of rats. Intra-arterial systolic, diastolic, mean and pulse pressures were measured in male Wistar rats aged 2, 4, 15 and 26 months. The passive mechanical properties of the wall of isolated perfused and pressurized arterial segments of mesenteric small arteries were also investigated. Intra-arterial systolic, diastolic and mean blood pressures tended to decrease with age and were significantly lower in the oldest rats (26-month-old group). Pulse pressure was significantly higher in the 15- and 26-month-old groups than in the two younger groups. Under isobaric conditions, increasing age is associated with an outward hypertrophic remodeling of the mesenteric arteries. Under relaxed conditions, incremental distensibility in response to increasing intravascular pressure did not change with aging. As a function of strain (under isometric conditions), stress shifted to the left as age increased, indicating an age-related vascular stiffening. Under isobaric conditions or in relation to wall stress, the elastic modulus was greater in the adult 15-month-old rats than in the younger rats. These findings suggest that distensibility seems to be preserved with aging, despite stiffness of the wall components, probably by arterial wall geometric adaptation, which limits the pulse pressure damage. It is interesting to note that elastic modulus in mesenteric arteries from the oldest rats (26-month-old), examined in relation to wall stress and intravascular pressure, did not differ from that of the youngest rats, thus suggesting that elasticity of wall components had been restored.Key words: age, arteries, elastic modulus, stiffness, pressure.

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Kastrup, J., T. Nørgaard, H. H. Parving, and N. A. Lassen. "Decreased distensibility of resistance vessels of the skin in type 1 (insulin-dependent) diabetic patients with microangiopathy." Clinical Science 72, no. 1 (January 1, 1987): 123–30. http://dx.doi.org/10.1042/cs0720123.

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1. The distensibility of the resistance vessels of the skin at the dorsum of the foot was determined in 11 long-term type 1 (insulin-dependent) diabetic patients with nephropathy and retinopathy, nine short-term type 1 diabetic patients without clinical microangiopathy and in nine healthy non-diabetic subjects. 2. Blood flow was measured by the local 133Xexenon washout technique in a vascular bed locally paralysed by the injection of histamine. Blood flow was measured before, during and after a 40 mmHg increase of the vascular transmural pressure, induced by head-up tilt. 3. The mean increase in blood flow during headup tilt was only 24% in diabetic subjects with and 48% in diabetic patients without clinical microangiopathy, compared with 79% in normal non-diabetic subjects (P < 0.0005 and P < 0.05, respectively). 4. An inverse correlation between microvascular distensibility and degree of hyalinosis of the terminal arterioles in biopsies from the skin was demonstrated (r = − 0.57, P < 0.001). 5. Our results suggest that terminal arteriolar hyalinosis reduces the microvascular distensibility and probably increases the minimal vascular resistance, thereby impeding hyperaemic responses.

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Guo, Hong, Jay D. Humphrey, and Michael J. Davis. "Effects of biaxial stretch on arteriolar function in vitro." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 5 (May 2007): H2378—H2386. http://dx.doi.org/10.1152/ajpheart.00810.2006.

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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.

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Zhang, Yunlong, Ken G. Stewart, and Sandra T. Davidge. "Endogenous estrogen mediates vascular reactivity and distensibility in pregnant rat mesenteric arteries." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 3 (March 1, 2001): H956—H961. http://dx.doi.org/10.1152/ajpheart.2001.280.3.h956.

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The role of estrogen in the maternal systemic cardiovascular adaptations during pregnancy is still controversial. Female Sprague-Dawley rats were implanted at day 14 of pregnancy with either a 50-mg tamoxifen pellet (estrogen receptor blocker, n = 10) or placebo pellet ( n = 10). Virgin female rats were a nonpregnant control ( n = 7). At days 20–22 of pregnancy, resistance-sized mesenteric arteries were mounted onto a dual-chamber arteriograph system. Pregnancy significantly blunted the pressor response to phenylephrine [measurement of the effective concentration that yielded 50% maximum response (EC50) values were 1.5 ± 0.22 vs. 0.69 ± 0.16 μM ( P < 0.05)] and enhanced vasodilation to ACh [EC50 = 1.13 ± 2.53 vs. 3.13 ± 6.04 nM ( P < 0.05)] compared with nonpregnant rats. However, tamoxifen treatment during pregnancy reversed these effects. Inhibition of nitric oxide (NO) synthase with N G-monomethyl-l-arginine (250 μM) shifted only the responses of the placebo-treated pregnant group to both phenylephrine and ACh. Arterial distensibility in the placebo-treated pregnant group was also significantly increased ( P < 0.05) compared with nonpregnant and tamoxifen-treated pregnant animals. In summary, endogenous estrogen during pregnancy increases NO-dependent modulation of vessel tone and arterial distensibility.

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Akkaya, Hasan, and Ertuğrul Emre Güntürk. "The relationship between coronary slow flow phenomenon and carotid femoral pulse wave velocity and aortic elastic properties." JRSM Cardiovascular Disease 9 (January 2020): 204800402097309. http://dx.doi.org/10.1177/2048004020973094.

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Introduction In this study, we aimed to investigate the relationship between coronary slow flow (CSF) and carotid-femoral pulse wave velocity (CFPWV). Methods 78 (27 women, mean age 43.95 ± 7.28) patients with CSF, and 70 (22 women, mean age 44.34 ± 7.08) healthy individuals were included in the study. Arterial stiffness measurement was performed to both groups via CFPWV, which is considered the gold standard. Aortic elastic properties (ASI-β and aortic distensibility) were evaluated in both groups. Results The CSF group had significantly higher CFPWV and aortic distensibility values and significantly lower ASI-β values compared to the control group. There was a positive correlation between TIMI frame count (TFC) obtained in all coronary arteries and CFPWV and aortic distensibility, and a negative correlation between TFC and ASI-β. It was determined that CFPWV predicted CSF with 97% specificity and 98% sensitivity at a 7.68 cut-off value (ROC area = 994, p < 0.001). ASI-β was determined to predict CSF with 64% specificity and 47% sensitivity at a 2.98 cut-off value (ROC area = 047, p < 0.001). Aortic distensibility was determined to predict CSF with 76% specificity and 79% sensitivity at a 3.94 cut-off value (ROC area = 706, p < 0.001). Conclusion Arterial stiffness increases in CSF patients, suggesting that CSF is a systemic pathology rather than a local disease and that a systemic cause such as atherosclerosis plays a role in etiology.

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Razavi, Hedi, Shahrzad Y. Zarafshar, Hirofumi Sawada, Charles A. Taylor, and Jeffrey A. Feinstein. "Quantitative characterization of postnatal growth trends in proximal pulmonary arteries in rats by phase-contrast magnetic resonance imaging." American Journal of Physiology-Lung Cellular and Molecular Physiology 301, no. 3 (September 2011): L368—L379. http://dx.doi.org/10.1152/ajplung.00069.2011.

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Malformations of the pulmonary arteries can increase right heart workload and result in morbidity, heart failure, and death. With the increased use of murine models to study these malformations, there is a pressing need for an accurate and noninvasive experimental technique that is capable of characterizing pulmonary arterial hemodynamics in these animals. We describe the growth trends of pulmonary arteries in 13 male Sprague-Dawley rats at 20, 36, 52, 100, and 160 days of age with the introduction of phase-contrast MRI as such a technique. PCMRI results correlated closely with cardiac output measurements by ultrasound echocardiography and with fluorescent microspheres in right-left lung flow split (flow partition). Mean flow, average cross-sectional area, distensibility, and shear rates for the right and left pulmonary arteries (RPA and LPA) were calculated. The RPA was larger and received more flow at all times than the LPA ( P < 0.0001). Right-left flow split did not change significantly with age, and arterial distensibility was not significantly different between RPA and LPA, except at 160 days ( P < 0.01). Shear rates were much higher for the LPA than the RPA ( P < 0.0001) throughout development. The RPA and LPA showed different structure-function relationships but obeyed similar allometric scaling laws, with scaling exponents comparable to those of the main pulmonary artery. This study is the first to quantitatively describe changes in RPA and LPA flows and sizes with development and to apply phase-contrast MRI techniques to pulmonary arteries in rats.

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Ussov, W. Yu, G. A. Ignatenko, T. A. Bergen, T. A. Shelkovnikova, K. R. Bril, V. V. Khovrin, A. S. Maksimova, O. I. Belichenko, and G. E. Trufanov. "Computational evaluation of mechano-elastic properties and of paramagnetic contrast enhancement of thoracic aortic wall in acute myocardial infarction and in non-coronarogenic myocardial damage, from the data of dynamic ECG-gated MRI (MR-elastometry)." Translational Medicine 8, no. 6 (February 22, 2022): 43–58. http://dx.doi.org/10.18705/2311-4495-2021-6-43-58.

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Background. The state of the aorta is a key factor in the prognosis of the patient’s life, since the distension of the ascending aorta in systole determines the blood supply to the myocardium in diastole. Paramagnetic contrast-enhanced MRI provides a reliable assessment of pathological neoangiogenesis, however, in fact, studies of the aorta are performed descriptively, without calculating mechanical strength and extensibility. Objective. To develop and clinically test on the patients with atherosclerotic lesions and myocarditis a method for quantitative assessment of extensibility and mechanical elasticity of the aortic wall.Design and methods. Were examined 12 patients with acute myocardial infarction with ST segment elevation, as a control group 11 patients without clinical and instrumental signs of atherosclerosis of large arteries and aorta. All underwent MRI of the chest and heart with paramagnetic contrast enhancement (PMCE) and ECG synchronization. The indices of aortic distensibility, distensibility normalized to pulse BP, Young’s modulus of the aortic wall, systolic distension of the ascending aorta (mL), index of strengthening of the aortic wall in PMCE were calculated.Results. Ascending aortic distensibility decreased in patients with myocarditis and acute infarction. Young’s modulus and distensibility of the ascending aorta significantly correlated with the value of the aortic wall enhancement index in PMCE. Myocardial damage in acute infarction and myocarditis was noted with a decrease in systolic expansion of the ascending aorta below 10 ml due to its reduced elasticity.Conclusion. There is a relationship between pathological accumulation of a paramagnet in the wall of the ascending aorta, a decrease in its elasticity, a decrease in the volume of systolic aortic dilation, and the development of hypoperfusion myocardial damage. Magnetic resonance elastometry of the aortic wall makes it possible to assess violations of aortic distensibility and predict the development of ischemic damage in the myocardium of the left ventricle.

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Lacolley, P., E. Glaser, P. Challande, P. Boutouyrie, J. P. Mignot, M. Duriez, B. Levy, M. Safar, and S. Laurent. "Structural changes and in situ aortic pressure-diameter relationship in long-term chemical-sympathectomized rats." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 2 (August 1, 1995): H407—H416. http://dx.doi.org/10.1152/ajpheart.1995.269.2.h407.

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This study determined the effects of long-term chemical sympathectomy with guanethidine (GN) on the mechanical properties and composition of the distal abdominal aorta in Wistar rats. GN was daily administered for 3 mo (3M-GN, from 1 to 12 wk), 5 wk (5W-GN, from 7 to 12 wk), and 8 days (8D-GN, from 11 to 12 wk). All experiments were performed at 12 wk of age to avoid age differences at examination. We used a high-resolution echo-tracking system to determine in situ, in the systolic-diastolic range, the aortic diameter-, compliance-, and distensibility-pressure curves in anesthetized rats. We observed an equivalent significant fall in the tyramine pressor response in all conscious GN-treated rats. Blood pressure was not affected by sympathectomy after 8 days and 5 wk of treatment but was significantly reduced in 3M-GN rats. Chronic sympathetic denervation increased aortic diameter and compliance in 8D-GN rats, compared with those obtained at the same distending pressure in control rats, suggesting vascular smooth muscle relaxation. In contrast, in 5W-GN and 3M-GN rats, the distensibility pressure-curves were significantly shifted toward lower levels of distensibility and pressure, indicating a decreased aortic distensibility at the same level of arterial pressure. Sympathectomy produced a significant reduction in the content of elastin, one of the most distensible components of the arterial wall in 5W-GN and 3M-GN rats. These results suggest that intact sympathetic nerves are necessary to maintain normal functional and structural properties of large arteries in rat. The reduction in aortic distensibility, in long-term sympathectomized rats, could have resulted from complex interactions between local aortic denervation, change in the set point of distending pressure, and changes in aortic smooth muscle tone and/or wall composition.

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Ghoneim, S. M., J. M. Chillon, and G. L. Baumbach. "Distensibility and wall composition of rat cerebral arterioles in hypertension induced by chronic blockade of nitric oxide synthase." Proceedings, annual meeting, Electron Microscopy Society of America 54 (August 11, 1996): 754–55. http://dx.doi.org/10.1017/s0424820100166233.

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We have previously reported that, during chronic hypertension, cerebral arterioles undergo hypertrophy of the vessel wall, accompanied by a paradoxical increase in passive distensibility. We have proposed that this increase may be due to a reduction in the proportion of nondistensible (collagen and basement membrane) to the distensible (smooth muscle, elastin and endothelium) components of the vessel wall. We have recently observed in stroke-prone spontaneously hypertensive rats(SHRSP), that an endothelium derived factor, endothelin, may contribute to hypertrophy, but not to increases in passive ditensibility, of cerebral arterioles vessel wall.The goal of this study was to examine wall mass, composition and passive ditensibility of cerebral arterioles in chronic hypertension induced by decreased availability of another endothelium derived factor, nitric oxide (NO).Four weeks old male Sprague-Dawley rats were treated with LG-nitro-L-arginine methyl ester (LNAME; 10 mg /kg/day) in the drinking water. We examined distensibility of maximally dilated cerebral arterioles in 4 months old Sprague-Dawley rats. Arterioles were then fixed at physiological pressure (2.25% gluterladehyde in 0.10 mol/L cacodylate buffer), the arteriolar segment used for distensibility measurements was removed then immerse fixed, rinsed briefly in 0.1 M cacodylate buffer, osmicated and processed routinely for electron microscopy (TEM).

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Herve, Philippe, Dominique Musset, Gérald Simonneau, Wiltz Wagner, and Pierre Duroux. "Almitrine Decreases the Distensibility of the Large Pulmonary Arteries in Man." Chest 96, no. 3 (September 1989): 572–77. http://dx.doi.org/10.1378/chest.96.3.572.

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SIMON, G. "Reduced distensibility and altered structure of arteries in salt-fed rats." American Journal of Hypertension 15, no. 4 (April 2002): A63. http://dx.doi.org/10.1016/s0895-7061(02)02438-x.

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Mehrotra, P. P., D. J. Patel, B. R. Coleman, R. J. Tearney, J. A. Diggs, L. N. Cothran, and C. L. Curry. "Distensibility of Small Pulmonary Blood Vessels." Journal of Biomechanical Engineering 115, no. 3 (August 1, 1993): 286–89. http://dx.doi.org/10.1115/1.2895488.

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Although vasomotor activity in small pulmonary vessels has been studied extensively in the past, using the concept of resistance to flow, information on the distensibility of these vessels is very sparse. In an attempt to reduce this deficit, we adapted a theoretical method developed for small systemic vessels, to estimate distensibility of pulmonary resistance vessels in experimental animals and man. Pressure-flow data from 11 dogs and 10 human subjects (5 control subjects and 5 patients with long-standing left heart failure) were used to calculate distensibility of small pulmonary vessels. The conductance, G, was calculated from these data as the ratio of blood flow to driving pressure. The slope of the relationship between the logarithm of G1/4 and the average distending pressure (ADP) provides a graphic picture of circumferential extensibility, E, defined as percent change in radius for an infinitesimal change in ADP. Results indicate that: (1) the value of E in dogs was 1.85 ± .40 mmHg−1 for the control state, which decreased to 1.45 ± .43 mmHg−1 during norepinephrine administration; however, the decrease in the value was not statistically significant (p = 0.53); (2) the value of E in control human subjects was 3.38 ± .47 mmHg−1 and the value of E in patients with left heart failure was −0.64 ± 0.39 mmHg−1; the difference was significant (P = .0001). Moreover, at a given ADP in the range of overlapping pressures, the “average” radius of small pulmonary vessels in patients with left heart failure was smaller than that in the control subjects; and (3) small pulmonary vessels were more distensible than both the small systemic vessels and the large pulmonary arteries.

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Vernhet, Hélène, Roland Demaria, Jean-Marie Juan, Marie-Claire Oliva-Lauraire, Jean-Paul Senac, and Michel Dauzat. "Arterial Stenting and Overdilation: Does it Change Wall Mechanics in Small-Caliber Arteries?" Journal of Endovascular Therapy 9, no. 6 (December 2002): 855–62. http://dx.doi.org/10.1177/152660280200900620.

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Purpose: To evaluate changes in arterial wall mechanics induced by stent overdilation in the rabbit aorta. Methods: Twenty New Zealand white rabbits had initial stent deployment (3-mm × 8-mm Multilink) at 10% overdilation. Group A (n=11) had no subsequent balloon expansion of the stent and Group B (n=9) had 30% overdilation of the stent. A noninvasive B-mode ultrasound examination coupled with image processing allowed the measurement of systolic and diastolic diameter and the calculation of diameter compliance (Cd) and distensibility coefficient (DC) as indexes of arterial wall biomechanics. Measurements were performed before stenting in the infrarenal aorta, after initial stenting, and after stent overdilation at 3 locations: upstream, at the stent level, and downstream from the stent. Results: Cd was significantly lower in the stented aorta after initial stenting (p<0.0001) and after stent overdilation (p<0.0001) than before stenting. At the stent level, Cd and DC were significantly lower than downstream (p<0.0001) or upstream (p<0.0001) from the stent after initial stenting, as well as after stent overdilation. Downstream from the stent, Cd and DC were significantly lower after stent overdilation than before stenting (p<0.05). Conclusions: Endovascular stenting of the rabbit aorta produces a significant decrease in arterial wall compliance and distensibility. Stent overdilation is responsible for a slight additional decrease of compliance downstream from the stent.

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Atkinson, J., P. Poitevin, J. M. Chillon, I. Lartaud, and B. Levy. "Vascular Ca overload produced by vitamin D3 plus nicotine diminishes arterial distensibility in rats." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 2 (February 1, 1994): H540—H547. http://dx.doi.org/10.1152/ajpheart.1994.266.2.h540.

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In humans, aging produces many structural changes in blood vessels, one of the most pronounced being arterial calcium overload. Simultaneously arteries become increasingly rigid. The slow evolution of the two processes renders it difficult to evaluate the importance of vascular calcium overload in the development of decreased compliance. To gain insight into this relationship, rapid vascular calcium overload was produced by treating young rats with vitamin D3 and nicotine. When rats were allowed 16 days or longer to recover from such treatment, analysis of plasma parameters revealed no overt toxicity, and growth rate was similar to that of controls. Pronounced calcium overload was seen primarily in compliance arteries. Changes in systemic arterial compliance, characteristic impedance, pulse-wave velocity, and carotid compliance all reflected a substantial increase in arterial rigidity. Linear regression analysis revealed significant correlations between the various indicators of arterial distensibility and arterial calcium content. In conclusion, treatment of young rats with vitamin D3 and nicotine may provide a suitable model with which to investigate how calcium overload is involved in the induration of compliance arteries.

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Lambert, J. "Familial hyperhomocysteinaemia and endothelium-dependent vasodilatation and arterial distensibility of large arteries." Cardiovascular Research 42, no. 3 (June 1999): 743–51. http://dx.doi.org/10.1016/s0008-6363(98)00338-1.

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Bortolotto, Luiz A., Olivier Hanon, Giovanna Franconi, Pierre Boutouyrie, Sylvie Legrain, and Xavier Girerd. "The Aging Process Modifies the Distensibility of Elastic but not Muscular Arteries." Hypertension 34, no. 4 (October 1999): 889–92. http://dx.doi.org/10.1161/01.hyp.34.4.889.

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Jaeckel, Marta, and Geza Simon. "Altered structure and reduced distensibility of arteries in Dahl salt-sensitive rats." Journal of Hypertension 21, no. 2 (February 2003): 311–19. http://dx.doi.org/10.1097/00004872-200302000-00022.

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The, Salem H. K., Elma J. Gussenhoven, Herman Pieterman, Luc M. A. B. van Bortel, Wenguang Li, Jos R. T. C. Roelandt, Pim de Feyter, and Hero van Urk. "Assessment of regional vascular distensibility in diseased iliofemoral arteries by intravascular ultrasound." Ultrasound in Medicine & Biology 21, no. 1 (January 1995): 17–24. http://dx.doi.org/10.1016/0301-5629(94)00099-9.

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Journal articles on the topic 'Distensibilità arteriosa'

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