Vessel growth and collapsible pressure-area relationship

1997 ◽  
Vol 273 (4) ◽  
pp. H2030-H2043 ◽  
Author(s):  
Gary Drzewiecki ◽  
Shawn Field ◽  
Issam Moubarak ◽  
John K.-J. Li
Keyword(s):  
High Pressures ◽  
Wall Thickening ◽  
Lumen Area ◽  
Jugular Veins ◽  
Wall Area ◽  
Wall Properties ◽  
Vessel Growth ◽  
Pressure Area ◽  
Lumen Narrowing ◽  
Wall Growth

The role that the pattern of vessel wall growth plays in determining pressure-lumen area (P-A) and pressure-compliance curves was examined. A P-A vessel model was developed that encompasses the complete range of pressure, including negative values, and accounts for size given the fixed length, nonlinear elastic wall properties, constant wall area, and collapse. Data were obtained from excised canine carotid and femoral arteries, jugular veins, and elastic tubing. The mean error of estimate was 8 mmHg for all vessels studied and 2 mmHg for blood vessels. The P-A model was employed to examine two patterns of arterial wall thickening, outward growth and remodeling (constant wall area), under the assumption of constant wall properties. The model predicted that only outward wall growth resets compliance such that it increases at a given arterial pressure, explaining previously contradictory data. In addition, it was found that outward wall growth increases the lumen area between normal and high pressures. Remodeling resulted in lumen narrowing and a decrease in compliance for positive pressures.

scholarly journals Chronic exposure to diesel exhaust may cause small airway wall thickening without lumen narrowing: a quantitative computerized tomography study in Chinese diesel engine testers

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Hong Liu ◽  
Jianyu Li ◽  
Qianli Ma ◽  
Jinglong Tang ◽  
Menghui Jiang ◽  
...  
Keyword(s):  
Diesel Engine ◽  
Diesel Exhaust ◽  
Airway Remodeling ◽  
Small Airway ◽  
Wall Thickening ◽  
Particulate Matters ◽  
Airway Wall ◽  
Wall Area ◽  
Lumen Narrowing ◽  
Area Percent

Abstract Background Diesel exhaust (DE) is a major source of ultrafine particulate matters (PM) in ambient air and contaminates many occupational settings. Airway remodeling assessed using computerized tomography (CT) correlates well with spirometry in patients with obstructive lung diseases. Structural changes of small airways caused by chronic DE exposure is unknown. Wall and lumen areas of 6th and 9th generations of four candidate airways were quantified using end-inhalation CT scans in 78 diesel engine testers (DET) and 76 non-DETs. Carbon content in airway macrophage (CCAM) in sputum was quantified to assess the dose-response relationship. Results Environmental monitoring and CCAM showed a much higher PM exposure in DETs, which was associated with higher wall area and wall area percent for 6th generation of airways. However, no reduction in lumen area was identified. No study subjects met spirometry diagnosis of airway obstruction. This suggested that small airway wall thickening without lumen narrowing may be an early feature of airway remodeling in DETs. The effect of DE exposure status on wall area percent did not differ by lobes or smoking status. Although the trend test was of borderline significance between categorized CCAM and wall area percent, subjects in the highest CCAM category has a 14% increase in wall area percent for the 6th generation of airways compared to subjects in the lowest category. The impact of DE exposure on FEV1 can be partially explained by the wall area percent with mediation effect size equal to 20%, Pperm = 0.028). Conclusions Small airway wall thickening without lumen narrowing may be an early image feature detected by CT and underlie the pathology of lung injury in DETs. The pattern of changes in small airway dimensions, i.e., thicker airway wall without lumen narrowing caused by occupational DE exposure was different to that (i.e., thicker airway wall with lumen narrowing) seen in our previous study of workers exposed to nano-scale carbon black aerosol, suggesting constituents other than carbon cores may contribute to such differences. Our study provides some imaging indications of the understanding of the pulmonary toxicity of combustion derived airborne particulate matters in humans.

scholarly journals Interaction between airway edema and lung inflation on responsiveness of individual airways in vivo

1997 ◽  
Vol 83 (2) ◽  
pp. 366-370 ◽  
Author(s):  
Robert H. Brown ◽  
Wayne Mitzner ◽  
Elizabeth M. Wagner
Keyword(s):  
Dose Response ◽  
Lung Volume ◽  
Bronchial Artery ◽  
Wall Thickening ◽  
Airway Wall ◽  
Lung Inflation ◽  
Wall Area ◽  
Airway Edema ◽  
Airway Constriction

Brown, Robert H., Wayne Mitzner, and Elizabeth M. Wagner.Interaction between airway edema and lung inflation on responsiveness of individual airways in vivo. J. Appl. Physiol. 83(2): 366–370, 1997.—Inflammatory changes and airway wall thickening are suggested to cause increased airway responsiveness in patients with asthma. In five sheep, the dose-response relationships of individual airways were measured at different lung volumes to methacholine (MCh) before and after wall thickening caused by the inflammatory mediator bradykinin via the bronchial artery. At 4 cmH2O transpulmonary pressure (Ptp), 5 μg/ml MCh constricted the airways to a maximum of 18 ± 3%. At 30 cmH2O Ptp, MCh resulted in less constriction (to 31 ± 5%). Bradykinin increased airway wall area at 4 and 30 cmH2O Ptp (159 ± 6 and 152 ± 4%, respectively; P < 0.0001). At 4 cmH2O Ptp, bradykinin decreased airway luminal area (13 ± 2%; P< 0.01), and the dose-response curve was significantly lower ( P = 0.02). At 30 cmH2O, postbradykinin, the maximal airway narrowing was not significantly different (26 ± 5%; P = 0.76). Bradykinin produced substantial airway wall thickening and slight potentiation of the MCh-induced airway constriction at low lung volume. At high lung volume, bradykinin increased wall thickness but had no effect on the MCh-induced airway constriction. We conclude that inflammatory fluid leakage in the airways cannot be a primary cause of airway hyperresponsiveness.

scholarly journals Relaxin regulates vascular wall remodeling and passive mechanical properties in mice

2011 ◽  
Vol 111 (1) ◽  
pp. 260-271 ◽  
Author(s):  
Dan O. Debrah ◽  
Julianna E. Debrah ◽  
Jamie L. Haney ◽  
Jonathan T. McGuane ◽  
Michael S. Sacks ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Knockout Mice ◽  
Total Protein ◽  
Vascular Remodeling ◽  
Circumferential Strain ◽  
Area Ratio ◽  
Lumen Area ◽  
Protein Ratio ◽  
Wall Area ◽  
Passive Compliance

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

Effects of lung volume, bronchoconstriction, and cigarette smoke on morphometric airway dimensions

1988 ◽  
Vol 64 (3) ◽  
pp. 913-919 ◽  
Author(s):  
A. L. James ◽  
P. D. Pare ◽  
J. C. Hogg
Keyword(s):  
Smooth Muscle ◽  
Cigarette Smoke ◽  
Lung Volume ◽  
Muscle Tone ◽  
Cigarette Smoke Exposure ◽  
Wall Thickening ◽  
Airway Wall ◽  
Lung Inflation ◽  
Wall Area ◽  
Airway Dimensions

To examine the role of airway wall thickening in the bronchial hyperresponsiveness observed after exposure to cigarette smoke, we compared the airway dimensions of guinea pigs exposed to smoke (n = 7) or air (n = 7). After exposure the animals were anesthetized with urethan, pulmonary resistance was measured, and the lungs were removed, distended with Formalin, and fixed near functional residual capacity. The effects of lung inflation and bronchoconstriction on airway dimensions were studied separately by distending and fixing lungs with Formalin at total lung capacity (TLC) (n = 3), 50% TLC (n = 3), and 25% TLC (n = 3) or near residual volume after bronchoconstriction (n = 3). On transverse sections of extraparenchymal and intraparenchymal airways the following dimensions were measured: the internal area (Ai) and internal perimeter (Pi), defined by the epithelium, and the external area (Ae) and external perimeter (Pe), defined by the outer border of smooth muscle. Airway wall area (WA) was then calculated, WA = Ae - Ai. Ai, Pe, and Ae decreased with decreasing lung volume and after bronchoconstriction. However, WA and Pi did not change significantly with lung volume or after bronchoconstriction. After cigarette smoke exposure airway resistance was increased (P less than 0.05); however, there was no difference in WA between the smoke- and air-exposed groups when the airways were matched by Pi. We conclude that Pi and WA are constant despite changes in lung volume and smooth muscle tone and that airway hyperresponsiveness induced by cigarette smoke is not mediated by increased airway wall thickness.

scholarly journals Airway wall attenuation: a biomarker of airway disease in subjects with COPD

2009 ◽  
Vol 107 (1) ◽  
pp. 185-191 ◽  
Author(s):  
George R. Washko ◽  
Mark T. Dransfield ◽  
Raúl San José Estépar ◽  
Alejandro Diaz ◽  
Shin Matsuoka ◽  
...  
Keyword(s):  
Lung Function ◽  
Wall Thickness ◽  
Airway Disease ◽  
Wall Thickening ◽  
Chronic Obstructive ◽  
Airway Wall ◽  
Wall Area ◽  
Computer Based ◽  
Structure Density ◽  
Contrast Reduction

The computed tomographic (CT) densities of imaged structures are a function of the CT scanning protocol, the structure size, and the structure density. For objects that are of a dimension similar to the scanner point spread function, CT will underestimate true structure density. Prior investigation suggests that this process, termed contrast reduction, could be used to estimate the strength of thin structures, such as cortical bone. In this investigation, we endeavored to exploit this process to provide a CT-based measure of airway disease that can assess changes in airway wall thickening and density that may be associated with the mural remodeling process in subjects with chronic obstructive pulmonary disease (COPD). An initial computer-based study using a range of simulated airway wall sizes and densities suggested that CT measures of airway wall attenuation could detect changes in both wall thickness and structure density. A second phantom-based study was performed using a series of polycarbonate tubes of known density. The results of this again demonstrated the process of contrast reduction and further validated the computer-based simulation. Finally, measures of airway wall attenuation, wall thickness, and wall area (WA) divided by total cross-sectional area, WA percent (WA%), were performed in a cohort of 224 subjects with COPD and correlated with spirometric measures of lung function. The results of this analysis demonstrated that wall attenuation is comparable to WA% in predicting lung function on univariate correlation and remain as a statistically significant correlate to the percent forced expiratory volume in 1 s predicted when adjusted for measures of both emphysema and WA%. These latter findings suggest that the quantitative assessment of airway wall attenuation may offer complementary information to WA% in characterizing airway disease in subjects with COPD.

scholarly journals Structural and hemodynamic changes in the carotid arteries in young healthy individuals with concentric remodeling of the left ventricle and with normal heart geometry

2019 ◽  
Vol 23 (3) ◽  
pp. 354-359
Author(s):  
B.V. Sheremta ◽  
N.Yu. Osovskaya
Keyword(s):  
Blood Pressure ◽  
Left Ventricle ◽  
Carotid Arteries ◽  
Blood Pressure Monitoring ◽  
Systolic Pressure ◽  
Wall Thickening ◽  
Healthy Individuals ◽  
Normal Heart ◽  
Jugular Veins ◽  
Study Results

Remodeling of the heart and blood vessels is a complex multifactorial process that determines the prognosis of a patient with different cardiovascular pathologies. The aim of this work is to study in a comparative aspect the features of the hemodynamics of the carotid arteries as marker vessels of the elastic type and the daily blood pressure profile in young healthy individuals with concentric remodeling of the left ventricle and with normal heart geometry. The study involved practically healthy individuals from 18 to 42, aged 25.3±0.6 years, 56 (73.7%) men and 20 (26.36%) women. All study participants were divided into two equal groups depending on the value of the relative wall thickness of the left ventricle (RTW) for 38 people: for RTW>0.42 (concentric remodeling of the left ventricle) and for RTW≤0.42 (normal geometry of the left ventricle). The following research methods were used: echocardiography, 24-hour blood pressure monitoring, duplex scanning of the neck vessels. Statistical analysis of the study results was calculated using the methods of variational statistics using the StatSoft complex “Statistica” v.12. Although the average daily values of blood pressure and the degree of its nightly decline in both groups did not differ significantly, the speed of the morning rise and the variability of systolic pressure were significantly higher in patients with concentric remodeling than without it. That is, even in the absence of symptoms of cardiovascular disease and a history of a rise in blood pressure, the hemodynamic factor of a fast morning increase in blood pressure can take part in the formation of changes in the geometry of the heart in practically healthy young people. Changes in the speed-time parameters of blood flow in the common carotid arteries in the absence of wall thickening (intima-media complex) and a parallel increase in the lumen of the internal jugular veins found in the study indicate structural and hemodynamic vascular remodeling associated with concentric remodeling of the left ventricle in young, practically healthy persons.

scholarly journals The BD2 domain of BRD4 is a determinant in EndoMT and vein graft neointima formation

2019 ◽  
Author(s):  
Mengxue Zhang ◽  
Bowen Wang ◽  
Go Urabe ◽  
Yitao Huang ◽  
Jorge Plutzky ◽  
...  
Keyword(s):  
Vein Graft ◽  
Dominant Negative ◽  
State Transitions ◽  
Wall Thickening ◽  
Neointima Formation ◽  
Neointimal Formation ◽  
Jugular Veins ◽  
Mesenchymal Transition

AbstractBackgroundVein-graft bypass is commonly performed to overcome atherosclerosis but is limited by high failure rates, principally due to neointimal wall thickening. Recent studies reveal that endothelial-mesenchymal transition (EndoMT) is critical for vein-graft neointima formation. BETs are a family of Bromo/ExtraTerminal domains-containing epigenetic reader proteins (BRD2, BRD3, BRD4). They bind acetylated histones through their unique tandem bromodomains (BD1, BD2), facilitating transcriptional complex formation and cell-state transitions. The role for BETs, including individual BRDs and their unique BDs, is not well understood in EndoMT and neointimal formation.Methods and ResultsRepression of BRD4 expression abrogated TGFβ1-induced EndoMT, with greater effects than BRD2 or BRD3 knockdown. An inhibitor selective for BD2 in all BETs, but not that for BD1, blocked EndoMT. Moreover, expression of a dominant-negative BRD4-specific BD2 fully abolished EndoMT. Concordantly, BRD4 knockdown repressed TGFβ1-stimulated increase of ZEB1 protein – a transcription factor integral in EndoMT. In vivo, lentiviral gene transfer of either BRD4 shRNA or dominant negative BRD4-specific BD2 mitigated neointimal development in rat jugular veins grafted to carotid arteries.ConclusionsOur data reveal the BD2 domain of BRD4 as a determinant driving EndoMT in vitro and neointimal formation in vivo. These findings provide new insight into BET biology, while offering prospects of specific BET domain targeting as an approach to limiting neointima and extending vein graft patency.

scholarly journals Small Airway Wall Thickening Assessed by Computerized Tomography Is Associated With Low Lung Function in Chinese Carbon Black Packers

2020 ◽  
Vol 178 (1) ◽  
pp. 26-35
Author(s):  
Xue Cao ◽  
Li Lin ◽  
Akshay Sood ◽  
Qianli Ma ◽  
Xiangyun Zhang ◽  
...  
Keyword(s):  
Lung Function ◽  
Carbon Black ◽  
Elemental Carbon ◽  
Airway Remodeling ◽  
Forced Expiratory Volume ◽  
Small Airway ◽  
Wall Thickening ◽  
Dependent Manner ◽  
Airway Wall ◽  
Wall Area

Abstract Nanoscale carbon black as virtually pure elemental carbon can deposit deep in the lungs and cause pulmonary injury. Airway remodeling assessed using computed tomography (CT) correlates well with spirometry in patients with obstructive lung diseases. Structural airway changes caused by carbon black exposure remain unknown. Wall and lumen areas of sixth and ninth generations of airways in 4 lobes were quantified using end-inhalation CT scans in 58 current carbon black packers (CBPs) and 95 non-CBPs. Carbon content in airway macrophage (CCAM) in sputum was quantified to assess the dose-response. Environmental monitoring and CCAM showed a much higher level of elemental carbon exposure in CBPs, which was associated with higher wall area and lower lumen area with no change in total airway area for either airway generation. This suggested small airway wall thickening is a major feature of airway remodeling in CBPs. When compared with wall or lumen areas, wall area percent (WA%) was not affected by subject characteristics or lobar location and had greater measurement reproducibility. The effect of carbon black exposure status on WA% did not differ by lobes. CCAM was associated with WA% in a dose-dependent manner. CBPs had lower FEV1 (forced expiratory volume in 1 s) than non-CBPs and mediation analysis identified that a large portion (41–72%) of the FEV1 reduction associated with carbon black exposure could be explained by WA%. Small airway wall thickening as a major imaging change detected by CT may underlie the pathology of lung function impairment caused by carbon black exposure.

Gene deletion of dopamine β-hydroxylase and α1-adrenoceptors demonstrates involvement of catecholamines in vascular remodeling

2004 ◽  
Vol 287 (5) ◽  
pp. H2106-H2114 ◽  
Author(s):  
Hua Zhang ◽  
Susanna Cotecchia ◽  
Steven A. Thomas ◽  
Akito Tanoue ◽  
Gozoh Tsujimoto ◽  
...  
Keyword(s):  
Wall Stress ◽  
In Vivo Studies ◽  
Wall Thickening ◽  
Lumen Area ◽  
Pharmacological Agents ◽  
Hypertrophic Growth ◽  
The Media ◽  
And Migration

In vitro studies have shown that stimulation of α1-adrenoceptors (ARs) directly induces proliferation, hypertrophy, and migration of arterial smooth muscle cells and adventitial fibroblasts. In vivo studies confirmed these findings and showed that catecholamine trophic activity becomes excessive after experimental balloon injury and contributes to neointimal growth, adventitial thickening, and lumen loss. However, past studies have been limited by selectivity of pharmacological agents. The aim of this study, in which mice devoid of norepinephrine and epinephrine synthesis [dopamine β-hydroxylase (DBH−/−)] or deficient in α1-AR subtypes expressed in murine carotid (α1B-AR−/− and α1D-AR−/−) were used, was to test the hypothesis that catecholamines contribute to wall hypertrophy after injury. At 3 wk after injury of wild-type mice, lumen area and carotid circumference increased significantly, and hypertrophy of media and adventitia was in excess of that needed to restore circumferential wall stress to normal. In DBH−/− and α1B-AR−/− mice, increases in lumen area, circumference, and hypertrophy of the media and adventitia were reduced by 50–91%, resulting in restoration of wall tension to nearly normal (DBH−/−) or normal (α1B-AR−/−). In contrast, in α1D-AR−/− mice, increases in lumen area, circumference, and wall hypertrophy were unaffected and wall thickening remained in excess of that required to return tension to normal. When examined 5 days after injury, proliferation and leukocyte infiltration were inhibited in DBH−/− mice. These studies suggest that the trophic effects of catecholamines are mediated primarily by α1B-ARs in mouse carotid and contribute to hypertrophic growth after vascular injury.

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