Relevant bibliographies by topics / Pulmonary artery stiffne

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Pulmonary artery stiffne'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Pulmonary artery stiffne"

1

LI, LIN, LIN HUA, HAIXIA ZHANG, and ZHICHENG LIU. "DIFFERENCES BETWEEN PULMONARY ARTERIAL AND AORTIC MATERIAL PROPERTIES." Journal of Mechanics in Medicine and Biology 15, no. 03 (June 2015): 1550019. http://dx.doi.org/10.1142/s0219519415500190.

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To investigate the differences of mechanical responses between pulmonary artery and aorta to different biaxial loading conditions, we simulated the process of human pulmonary artery and aorta subjected to biaxial loading based on four-family fiber strain density function model determined from uniaxial extension data of arterial walls. It was shown that different stress–strain curves of pulmonary artery and aorta under biaxial loading conditions: different loading ratios between the loads in two perpendicular directions and displacement-controlled equibiaxial stretch. Tissue stiffness, defined as the first derivative of the stress–strain response at a strain point, of human pulmonary artery and aorta were obtained when they were subjected to biaxial loads (systemic pressure). The two-dimensional mechanical response of artery can be acquired by determination of the four-family fiber strain density function model of the tissue based on uniaxial extensile data. There are differences between material properties of pulmonary artery and aorta: aorta is stiffer circumferentially than longitudinally, and pulmonary artery is more compliant circumferentially than longitudinally.
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Lammers, Steven R., Phil H. Kao, H. Jerry Qi, Kendall Hunter, Craig Lanning, Joseph Albietz, Stephen Hofmeister, Robert Mecham, Kurt R. Stenmark, and Robin Shandas. "Changes in the structure-function relationship of elastin and its impact on the proximal pulmonary arterial mechanics of hypertensive calves." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 4 (October 2008): H1451—H1459. http://dx.doi.org/10.1152/ajpheart.00127.2008.

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Extracellular matrix remodeling has been proposed as one mechanism by which proximal pulmonary arteries stiffen during pulmonary arterial hypertension (PAH). Although some attention has been paid to the role of collagen and metallomatrix proteins in affecting vascular stiffness, much less work has been performed on changes in elastin structure-function relationships in PAH. Such work is warranted, given the importance of elastin as the structural protein primarily responsible for the passive elastic behavior of these conduit arteries. Here, we study structure-function relationships of fresh arterial tissue and purified arterial elastin from the main, left, and right pulmonary artery branches of normotensive and hypoxia-induced pulmonary hypertensive neonatal calves. PAH resulted in an average 81 and 72% increase in stiffness of fresh and digested tissue, respectively. Increase in stiffness appears most attributable to elevated elastic modulus, which increased 46 and 65%, respectively, for fresh and digested tissue. Comparison between fresh and digested tissues shows that, at 35% strain, a minimum of 48% of the arterial load is carried by elastin, and a minimum of 43% of the change in stiffness of arterial tissue is due to the change in elastin stiffness. Analysis of the stress-strain behavior revealed that PAH causes an increase in the strains associated with the physiological pressure range but had no effect on the strain of transition from elastin-dominant to collagen-dominant behavior. These results indicate that mechanobiological adaptations of the continuum and geometric properties of elastin, in response to PAH, significantly elevate the circumferential stiffness of proximal pulmonary arterial tissue.
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Mulchrone, A., H. Moulton, M. W. Eldridge, and N. C. Chesler. "Susceptibility to high-altitude pulmonary edema is associated with increased pulmonary arterial stiffness during exercise." Journal of Applied Physiology 128, no. 3 (March 1, 2020): 514–22. http://dx.doi.org/10.1152/japplphysiol.00153.2019.

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High-altitude pulmonary edema (HAPE), a reversible form of capillary leak, is a common consequence of rapid ascension to high altitude and a major cause of death related to high-altitude exposure. Individuals with a prior history of HAPE are more susceptible to future episodes, but the underlying risk factors remain uncertain. Previous studies have shown that HAPE-susceptible subjects have an exaggerated pulmonary vasoreactivity to acute hypoxia, but incomplete data are available regarding their vascular response to exercise. To examine this, seven HAPE-susceptible subjects and nine control subjects (HAPE-resistant) were studied at rest and during incremental exercise at sea level and at 3,810 m altitude. Studies were conducted in both normoxic (inspired Po2 = 148 Torr) and hypoxic (inspired Po2 = 91 Torr) conditions at each location. Here, we report an expanded analysis of previously published data, including a distensible vessel model that showed that HAPE-susceptible subjects had significantly reduced small distal artery distensibility at sea level compared with HAPE-resistant control subjects [0.011 ± 0.001 vs. 0.021 ± 0.002 mmHg−1; P < 0.001). Moreover, HAPE-susceptible subjects demonstrated constant distensibility over all conditions, suggesting that distal arteries are maximally distended at rest. Consistent with having increased distal artery stiffness, HAPE-susceptible subjects had greater increases in pulmonary artery pulse pressure with exercise, which suggests increased proximal artery stiffness. In summary, HAPE-susceptible subjects have exercise-induced increases in proximal artery stiffness and baseline increases in distal artery stiffness, suggesting increased pulsatile load on the right ventricle. NEW & NOTEWORTHY In comparison to subjects who appear resistant to high-altitude pulmonary edema, those previously symptomatic show greater increases in large and small artery stiffness in response to exercise. These differences in arterial stiffness may be a risk factor for the development of high-altitude pulmonary edema or evidence that consequences of high-altitude pulmonary edema are long-lasting after return to sea level.
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Stack, Alice, Frederik J. Derksen, Kurt J. Williams, N. Edward Robinson, and William F. Jackson. "Lung region and racing affect mechanical properties of equine pulmonary microvasculature." Journal of Applied Physiology 117, no. 4 (August 15, 2014): 370–76. http://dx.doi.org/10.1152/japplphysiol.00314.2014.

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Exercise-induced pulmonary hemorrhage is a performance-limiting condition of racehorses associated with severe pathology, including small pulmonary vein remodeling. Pathology is limited to caudodorsal (CD) lung. Mechanical properties of equine pulmonary microvasculature have not been studied. We hypothesized that regional differences in pulmonary artery and vein mechanical characteristics do not exist in control animals, and that racing and venous remodeling impact pulmonary vein mechanical properties in CD lung. Pulmonary arteries and veins [range of internal diameters 207–386 ± 67 μm (mean ± SD)] were harvested from eight control and seven raced horses. With the use of wire myography, CD and cranioventral (CV) vessels were stretched in 10-μm increments. Peak wall tension was plotted against changes in diameter (length). Length-tension data were compared between vessel type, lung region, and horse status (control and raced). Pulmonary veins are stiffer walled than arteries. CD pulmonary arteries are stiffer than CV arteries, whereas CV veins are stiffer than CD veins. Racing is associated with increased stiffness of CD pulmonary veins and, to a lesser extent, CV arteries. For example, at 305 μm, tension in raced and control CD veins is 27.74 ± 2.91 and 19.67 ± 2.63 mN/mm (means ± SE; P < 0.05, Bonferroni's multiple-comparisons test after two-way ANOVA), and 16.12 ± 2.04 and 15.07 ± 2.47 mN/mm in raced and control CV arteries, respectively. This is the first report of an effect of region and/or exercise on mechanical characteristics of small pulmonary vessels. These findings may implicate pulmonary vein remodeling in exercise-induced pulmonary hemorrhage pathogenesis.
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Nemes, Attila, and Tamás Forster. "Evaluation of pulmonary arterial stiffness using routine clinical imaging methods." Orvosi Hetilap 154, no. 49 (December 2013): 1931–33. http://dx.doi.org/10.1556/oh.2013.29767.

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Recently, there has been much debate about pulmonary hypertension due to modern therapeutic options available. Arterial hypertension is frequently associated with stiffening of a given artery. The aim of the present review is to present clinical imaging methods for the evaluation of the function and stiffness of the pulmonary artery. Orv. Hetil., 154(49), 1931–1933.
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Su, Junjing, Alun D. Hughes, Ulf Simonsen, Jens Erik Nielsen-Kudsk, Kim H. Parker, Luke S. Howard, and Soren Mellemkjaer. "Impact of pulmonary endarterectomy on pulmonary arterial wave propagation and reservoir function." American Journal of Physiology-Heart and Circulatory Physiology 317, no. 3 (September 1, 2019): H505—H516. http://dx.doi.org/10.1152/ajpheart.00181.2019.

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High wave speed and large wave reflection in the pulmonary artery have previously been reported in patients with chronic thromboembolic pulmonary hypertension (CTEPH). We assessed the impact of pulmonary endarterectomy (PEA) on pulmonary arterial wave propagation and reservoir function in patients with CTEPH. Right heart catheterization was performed using a combined pressure and Doppler flow sensor-tipped guidewire to obtain simultaneous pressure and flow velocity measurements in the pulmonary artery in eight patients with CTEPH before and 3 mo after PEA. Wave intensity and reservoir-excess pressure analyses were then performed. Following PEA, mean pulmonary arterial pressure (PAPm; ∼49 vs. ∼32 mmHg), pulmonary vascular resistance (PVR; ∼11.1 vs. ∼5.1 Wood units), and wave speed (∼16.5 vs. ∼8.1 m/s), i.e., local arterial stiffness, markedly decreased. The changes in the intensity of the reflected arterial wave and wave reflection index (pre: ∼28%; post: ∼22%) were small, and patients post-PEA with and without residual pulmonary hypertension (i.e., PAPm ≥ 25 mmHg) had similar wave reflection index (∼20 vs. ∼23%). The reservoir and excess pressure decreased post-PEA, and the changes were associated with improved right ventricular afterload, function, and size. In conclusion, although PVR and arterial stiffness decreased substantially following PEA, large wave reflection persisted, even in patients without residual pulmonary hypertension, indicating lack of improvement in vascular impedance mismatch. This may continue to affect the optimal ventriculoarterial interaction, and further studies are warranted to determine whether this contributes to persistent symptoms in some patients. NEW & NOTEWORTHY We performed wave intensity analysis in the pulmonary artery in patients with chronic thromboembolic pulmonary hypertension before and 3 mo after pulmonary endarterectomy. Despite substantial reduction in pulmonary arterial pressures, vascular resistance, and arterial stiffness, large pulmonary arterial wave reflection persisted 3 mo postsurgery, even in patients without residual pulmonary hypertension, suggestive of lack of improvement in vascular impedance mismatch.
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Woodcock, Chen-Shan Chen, Neha Hafeez, Adam Handen, Ying Tang, Lloyd D. Harvey, Leonard E. Estephan, Gil Speyer, Seungchan Kim, Thomas Bertero, and Stephen Y. Chan. "Matrix stiffening induces a pathogenic QKI-miR-7-SRSF1 signaling axis in pulmonary arterial endothelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 320, no. 5 (May 1, 2021): L726—L738. http://dx.doi.org/10.1152/ajplung.00407.2020.

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Pulmonary arterial hypertension (PAH) refers to a set of heterogeneous vascular diseases defined by elevation of pulmonary arterial pressure (PAP) and pulmonary vascular resistance (PVR), leading to right ventricular (RV) remodeling and often death. Early increases in pulmonary artery stiffness in PAH drive pathogenic alterations of pulmonary arterial endothelial cells (PAECs), leading to vascular remodeling. Dysregulation of microRNAs can drive PAEC dysfunction. However, the role of vascular stiffness in regulating pathogenic microRNAs in PAH is incompletely understood. Here, we demonstrated that extracellular matrix (ECM) stiffening downregulated miR-7 levels in PAECs. The RNA-binding protein quaking (QKI) has been implicated in the biogenesis of miR-7. Correspondingly, we found that ECM stiffness upregulated QKI, and QKI knockdown led to increased miR-7. Downstream of the QKI-miR-7 axis, the serine and arginine-rich splicing factor 1 (SRSF1) was identified as a direct target of miR-7. Correspondingly, SRSF1 was reciprocally upregulated in PAECs exposed to stiff ECM and was negatively correlated with miR-7. Decreased miR-7 and increased QKI and SRSF1 were observed in lungs from patients with PAH and PAH rats exposed to SU5416/hypoxia. Lastly, miR-7 upregulation inhibited human PAEC migration, whereas forced SRSF1 expression reversed this phenotype, proving that miR-7 depended upon SRSF1 to control migration. In aggregate, these results define the QKI-miR-7-SRSF1 axis as a mechanosensitive mechanism linking pulmonary arterial vascular stiffness to pathogenic endothelial function. These findings emphasize implications relevant to PAH and suggest the potential benefit of developing therapies that target this miRNA-dependent axis in PAH.
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Gan, C. Tji-Joong, Jan-Willem Lankhaar, Nico Westerhof, J. Tim Marcus, Annemarie Becker, Jos W. R. Twisk, Anco Boonstra, Pieter E. Postmus, and Anton Vonk-Noordegraaf. "Noninvasively Assessed Pulmonary Artery Stiffness Predicts Mortality in Pulmonary Arterial Hypertension." Chest 132, no. 6 (December 2007): 1906–12. http://dx.doi.org/10.1378/chest.07-1246.

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9

Dodson, R. Blair, Matthew R. Morgan, Csaba Galambos, Kendall S. Hunter, and Steven H. Abman. "Chronic intrauterine pulmonary hypertension increases main pulmonary artery stiffness and adventitial remodeling in fetal sheep." American Journal of Physiology-Lung Cellular and Molecular Physiology 307, no. 11 (December 1, 2014): L822—L828. http://dx.doi.org/10.1152/ajplung.00256.2014.

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Persistent pulmonary hypertension of the newborn (PPHN) is a clinical syndrome that is characterized by high pulmonary vascular resistance due to changes in lung vascular growth, structure, and tone. PPHN has been primarily considered as a disease of the small pulmonary arteries (PA), but proximal vascular stiffness has been shown to be an important predictor of morbidity and mortality in other diseases associated with pulmonary hypertension (PH). The objective of this study is to characterize main PA (MPA) stiffness in experimental PPHN and to determine the relationship of altered biomechanics of the MPA with changes in extracellular matrix (ECM) content and orientation of collagen and elastin fibers. MPAs were isolated from control and PPHN fetal sheep model and were tested by planar biaxial testing to measure stiffness in circumferential and axial vessel orientations. Test specimens were fixed for histological assessments of the vascular wall ECM constituents collagen and elastin. MPAs from PPHN sheep had increased mechanical stiffness ( P < 0.05) and altered ECM remodeling compared with control MPA. A constitutive mathematical model and histology demonstrated that PPHN vessels have a smaller contribution of elastin and a greater role for collagen fiber engagement compared with the control arteries. We conclude that exposure to chronic hemodynamic stress in late-gestation fetal sheep increases proximal PA stiffness and alters ECM remodeling. We speculate that proximal PA stiffness further contributes to increased right ventricular impedance in experimental PPHN, which contributes to abnormal transition of the pulmonary circulation at birth.
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Stevens, Gerin R., Ana Garcia-Alvarez, Sheila Sahni, Mario J. Garcia, Valentin Fuster, and Javier Sanz. "RV Dysfunction In Pulmonary Hypertension Is Independently Related To Pulmonary Artery Stiffness." JACC: Cardiovascular Imaging 5, no. 4 (April 2012): 378–87. http://dx.doi.org/10.1016/j.jcmg.2011.11.020.

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Dissertations / Theses on the topic "Pulmonary artery stiffne"

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ALBERTI, ELENA. "EVALUATION OF PULMONARY ARTERY STIFFNESS IN ASTHMA AFFECTED HORSES." Doctoral thesis, Università degli Studi di Milano, 2022. http://hdl.handle.net/2434/916663.

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The present research evaluated Pulmonary Artery Stiffness (PAS) and right ventricular systolic time intervals (RVSTIs) in horses with mild/moderate (MEA) and severe (SEA) equine asthma and in healthy horses. In human medicine, PAS is a pulsed-wave (PW) Doppler echocardiographic parameter useful in assessing an increase in pulmonary artery stiffness due to remodeling of the vessel wall caused by chronic diseases. Moreover, PAS in humans is used as an early indicator of pulmonary hypertension. RVSTIs, such as acceleration time (AT), ejection time (ET) and acceleration time index (AT/ET), are other PW Doppler parameters useful for the evaluation of changes in the pulmonary vascular bed. Like human asthma, equine asthma is able to induce remodeling of the pulmonary artery wall even in horses, leading to a decreased pulmonary artery elasticity and consequently pulmonary hypertension. Therefore, it is conceivable that PAS could be a useful parameter also in horses. However, there are no studies on PAS in veterinary medicine. The aims of this research were: to assess feasibility of PAS in horses, to evaluate possible influence of age, bodyweight, sex and heart rate on PAS and RVSTIs, to investigate possible differences between healthy, MEA and SEA horses regarding those parameters, to evaluate possible correlation between PAS and RVSTIs and ratio of pulmonary artery diameter to aorta diameter (PAD/AOD) and to determine PAS and AT cut-off values for diagnosis of SEA. Echocardiographic examination and PW Doppler of the pulmonary flow were performed in 23 MEA affected horses, 15 SEA affected horses and 15 healthy horses. Results demonstrated that PAS can been measured consistently in horses and that, as well as RVSTIs, it is not influenced by age, bodyweight, sex and heart rate. Moreover, a significant higher PAS and lower RVSTIs were detected in SEA affected horses compared to healthy subjects and MEA affected ones. In addition, considering the whole sample, a positive correlation between PAS and PAD/AOD and a negative correlation between AT or AT/ET and PAD/AOD were found. These findings, in association with several similarities between equine asthma and human asthma, suggest that these parameters could be correlated to pulmonary pressure even in horses. Finally, this study determined that a PAS value of 8.18 kHz/sec and a AT value of 0.202 sec are the best cut-off values, with a very high sensitivity (PAS: 93.33%; AT: 86.67%) and specificity (PAS: 86.84%; AT: 89.47%), for the diagnosis of SEA.
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Book chapters on the topic "Pulmonary artery stiffne"

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Corcoran, Alexis M., Rakhshinda Rehman, Marcy Maracle, Piera Sosa, Paul B. Dieffenbach, and Laura E. Fredenburgh. "Biologic mechanisms and consequences of pulmonary artery stiffening in pulmonary hypertension." In Textbook of Arterial Stiffness and Pulsatile Hemodynamics in Health and Disease, 917–34. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-323-91391-1.00057-1.

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Niki, Kiyomi, and Motoaki Sugawara. "Evaluation of the Effect of Increased Arterial Stiffness on Ejection Performance and Pulmonary Arterial Pressure in Primary Mitral Regurgitation and Prediction of Ejection Fraction after Surgery: Analysis Using Wave Intensity." In The Current Perspectives on Coronary Artery Bypass Grafting. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.89458.

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Conference papers on the topic "Pulmonary artery stiffne"

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Kobs, Ryan W., Nidal E. Muvarak, and Naomi C. Chesler. "Hypoxia-Induced Changes in the Mechanical Properties of the Mouse Pulmonary Artery." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43086.

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Hypobaric hypoxia produces pulmonary hypertension in mice which causes pulmonary vascular remodeling. To study the biomechanics of this process, mice were exposed to hypoxia for 0-(control), 10-, and 15-days. Using a pressurized arteriograph system, mechanical properties of the main pulmonary artery were measured and compared to the biological changes in the vessel wall measured histologically. 10- and 15-day hypoxic vessels were significantly stiffer when compared to 0-day vessels. This stiffness correlated with greater elastin and collagen content in the vessel wall.
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Zhao, Shijia, Linxia Gu, James M. Hammel, and Haili Lang. "Mechanical Behavior of Porcine Pulmonary Artery." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-39012.

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Proper characterization of the material properties of pulmonary arterial tissue is needed for many medical applications. The objective of this study was to investigate the stress-strain relationship and characterize the nonlinear elastic behavior of porcine pulmonary arteries; thus, uniaxial tension tests and cyclic loading-unloading tests were conducted on healthy porcine pulmonary arterial tissue. In these experiments, pulmonary arteries from different piglets and a commercial pulmonary valved conduit, called “Contegra 200”, were subjected to uniaxial tension. Results demonstrated a higher stiffness along the circumferential direction than the axial direction. The “Contegra 200” was much suffer than real pulmonary arterial tissue along the axial direction and had a similar stiffness to natural tissue along the circumferential direction within physiological stretch ranges, which is less than 40% strain. Elastic hysteresis was observed from cyclic loading-unloading tests, which indicates that more energy was required during the loading than the unloading. A nonlinear hyperelastic model based on second order polynomial constitutive equation was derived from average values of the test data along both axial and circumferential directions. The material model could be used in numerical analysis of pulmonary arterial response and facilitate the design of intravascular devices.
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Ooi, Chen Yen, and Naomi C. Chesler. "The Role of Collagen in Pulmonary Hypertension-Induced Large Artery Stiffening." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192951.

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Hypoxic pulmonary hypertension (HPH) leads to stiffening of large pulmonary arteries, which affects right ventricular afterload. We hypothesized that vascular collagen accumulation is the major cause of large pulmonary artery (PA) stiffening in HPH. We tested this hypothesis with transgenic mice that produce collagen type I resistant to degradation (Col1a1R/R) and wild type littermate controls (Col1a1+/+) exposed to hypoxia and allowed to recover. Pressure-diameter testing on left PAs demonstrated that stiffness in control mice increased with hypoxia and decreased with recovery (p < 0.05). Preliminary tests in degradation-resistant mice suggest that PA stiffness decreases less with recovery than in controls. Quantitative measurements of vascular collagen content in right PAs are planned to develop statistical correlations between structure and function.
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Liu, Aiping, Lian Tian, Diana M. Tabima, and Naomi C. Chesler. "Sex Differences in Right Ventricular-Vascular Coupling and Pulmonary Artery Impedance in Response to Chronic Hypoxia and Recovery." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80835.

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Pulmonary artery hypertension (PAH) is a female dominant disease (the female-to-male ratio is 4:1), characterized by small distal pulmonary arterial narrowing and large proximal arterial stiffening, which increase right ventricle (RV) afterload and ultimately lead to RV failure [1,2]. Our recent studies have shown that collagen accumulation induced by chronic hypoxia increases the stiffness of the large extralobar pulmonary arteries (PAs) [3], and affects pulmonary vascular impedance (PVZ) [4]. The role of collagen in the female predominance in developing PAH has not been explored to date.
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Wang, Zhijie, Roderic S. Lakes, and Naomi C. Chesler. "Changes in Conduit Pulmonary Arterial Static and Dynamic Mechanical Properties During Severe Hypoxic Pulmonary Hypertension." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80382.

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Pulmonary hypertension (PH) is a complex disorder that manifests as abnormally high blood pressure in the vasculature of the lungs. The chronic structural and mechanical changes in the proximal pulmonary artery (PA) associated with PH include smooth muscle cell hypertrophy and proliferation, accumulation of extracellular matrix (ECM) protein and increased stiffness1–4. Recent evidence has shown that conduit PA stiffness is a strong predictor of mortality in pulmonary arterial hypertension5,6. This suggests a potential association between large PA biomechanics and right ventricle failure.
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Hayman, Danika M., Merry L. Lindsey, and Hai-Chao Han. "The Effect of Pulse Pressure on Arterial Wall Permeability and Stiffness." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53730.

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Artery pulse pressure has been increasingly studied as a factor that can predict overall health. In people younger than 50 the mean pressure tends to increase with age while the pulse pressure remains constant; however, in patients older than 50 the systolic pressure continues to increase while the diastolic pressure starts to decrease resulting in a widened pulse pressure [1]. Stiffening of the artery wall and changes in the ejection fraction from the heart both alter the pulse pressure. Decreases in pulse pressure can also be caused by disease, but mostly this change is caused by the use of steady flow left ventricular assist devices or cardio pulmonary bypass machines [2]. These changes in pulse pressure affect the flow of blood throughout the body and can have effects on the function of organs outside of the cardiovascular system. However the immediate effects of these changes in pulse pressure are not well understood. This study examines the changes in the mechanical properties of the artery wall, arterial permeability and protein levels that occur immediately after a change in pulse pressure.
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Domingo, Enric, Juan C. Grignola, Rio Aguilar, Manuel Vazquez, Manuel Lopez-Messeguer, Carlos Bravo, and Antonio Roman. "Correlation Between Local Pulmonary Artery Stiffness And The Acute Vasoreactivity Test In Pulmonary Arterial Hypertension." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5745.

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Lammers, Steven, Tosin Feyintola, Kendall Hunter, Emily Gibson, Tim Lei, Phil Kao, H. Jerry Qi, Craig Lanning, Robin Shandas, and Kurt Stenmark. "Microstructural Changes in Collagen and Elastin and Their Impact on the Mechanics of the Pulmonary Artery in Hypertension." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53958.

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In pulmonary arteries (PA), mechanical function is largely driven by the underlying microstructure of the structural proteins collagen and elastin, which reside within the extracellular matrix (ECM) of the arterial tissue. It has long been established that much of the mechanical non-linearity associated with arterial tissue is the result of collagen mechanics. Arterial collagen is arranged within the vascular wall as tortuous fibrils with a bulk fiber orientation of roughly helical configuration. When arterial tissue is deformed, these collagen fibers become straightened in the direction of applied load. At some critical deformation, termed the transition stretch (λTrans), collagen fibers begin to carry load, thus significantly altering material stiffness. This in turn gives rise to the non-linear force-stretch (F-λ) response typical of these tissues, Figure 1. We have recently found that λTrans is significantly reduced in the hypoxia-induced pulmonary hypertensive (PH) rat model. We therefore propose that this model constitutes an ideal system to study the effect of collagen microstructure on the mechanics of arterial tissues in response to PH vascular remodeling. We hypothesize that quantitative characterization of collagen microstructure will predict pulmonary artery (PA) λTrans within this model system. By directly relating collagen microstructural changes to bulk tissue mechanics in response to PH-induced vascular remodeling we can better understand how changes in collagen structure impact pulmonary hemodynamic capacitance, a major component of cardiac load and contributing factor to right heart failure.
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Reusser, Mark A., Steve Lammers, Kurt Stenmark, and Kendall Hunter. "Changes In Collagen Engagement Strain And Stiffness In The Posthilar Conduit Pulmonary Artery As A Result Of Pulmonary Hypertension." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1243.

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Vural, Mustafa G., Esra Bilgin, Özge Özcan, Ahmet G. Ertem, Göksel Cagirci, Hikmet Firat, Ekrem Yeter, sadık ardıç, and Ramazan Akdemir. "Increased Stiffness And Decreased Elasticity In Pulmonary Artery In Patients With Obstructive Sleep Apnea Syndrome." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2213.

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