Pulmonary arterial wall thickness in Eisenmenger Syndrome: Prospective, cross-sectional, controlled clinical trial

2015 ◽  
Vol 50 (12) ◽  
pp. 1253-1261 ◽  
Author(s):  
Nazmi Narin ◽  
Abdullah Ozyurt ◽  
Suleyman Sunkak ◽  
Ali Baykan ◽  
Mustafa Argun ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Wall Thickness ◽  
Arterial Wall ◽  
Controlled Clinical Trial ◽  
Eisenmenger Syndrome ◽  
Cross Sectional ◽  
Arterial Wall Thickness ◽  
Pulmonary Arterial

Hypoxia-Induced Pulmonary Arterial Hypertension: The Role of TLR4

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 1146-1146
Author(s):  
Liping Ma ◽  
Jianxing Chang ◽  
Hui Wu ◽  
Yabing Chen
Keyword(s):  
Reactive Oxygen Species ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Wall Thickness ◽  
Arterial Wall ◽  
Pulmonary Vasculature ◽  
Oxygen Species ◽  
Arterial Wall Thickness ◽  
Pulmonary Arterial

Abstract Abstract 1146 Pulmonary arterial hypertension (PAH) is often as a result of COPD and contributes to morbidity and mortality of chronic cor pulmonale. Hypoxemia is its main clinical features. The toll-like receptors are a group of type I transmembrane proteins that play a central role in specific recognition of pathagen-associated molecular patterns and are critical for the induction of innate immunity and inflammation. Expression of these innate immune receptors, especially TLR4 in healthy and pathological arteries has implicated its role in the homeostasis of vasculature. Chronic hypoxia-induced PAH is mediated by increased production of reactive oxygen species (ROS). ROS have been linked to activation of toll-like receptor 4 (TLR4) signaling. The present studies investigated the role of TLR4 in the pathogenesis PAH and the underlying mechanisms. In vitro, pulmonary arterial smooth muscle cells (PASMC) derived from TLR4−/− mice exhibited increased production of intracellular reactive oxygen species (ROS). Furthermore, under hypoxia, the expression of TLR4 in PASMC from WT mice was decreased, ROS production in PASMC from WT mice were increased, suggesting down-regulation of TLR4 may contribute to hypoxia-induced PAH. Using a hypoxia-induced PAH model, we found that hypoxia induced PAH and increased pulmonary arterial wall thickness in wild type (WT) mice. In contrast, mice deficient in TLR4 spontaneously developed PAH and increased pulmonary arterial wall thickness, which were not further enhanced by hypoxia. Consistent with the development of PAH in TLR4−/− mice, echocardiography confirmed right ventricular hypertrophy and decreased pulmonary arterial acceleration time compared to WT mice. Above results suggest that TLR4 plays an important role in maintaining normal pulmonary vasculature, and that hypoxia induces PAH via TLR4. In short, these studies demonstrate an important role of TLR4 in maintaining normal pulmonary vasculature and in the development of hypoxia-induced PAH. Genetic ablation of TLR4 and inhibition of TLR4 expression by hypoxia induces PASMC proliferation and vascular remodeling, in association with redox signaling in the pathogenesis of PAH. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Linked opening angle and histological and mechanical aspects of the proximal pulmonary arteries of healthy and pulmonary hypertensive rats and calves

2011 ◽  
Vol 301 (5) ◽  
pp. H1810-H1818 ◽  
Author(s):  
Lian Tian ◽  
Steven R. Lammers ◽  
Philip H. Kao ◽  
Mark Reusser ◽  
Kurt R. Stenmark ◽  
...  
Keyword(s):  
Mechanical Behavior ◽  
Wall Thickness ◽  
Arterial Wall ◽  
Chronic Hypoxia ◽  
Pulmonary Arteries ◽  
Opening Angle ◽  
Histological Structure ◽  
Arterial Remodeling ◽  
Stiffness Ratio ◽  
Arterial Wall Thickness

Understanding how arterial remodeling changes the mechanical behavior of pulmonary arteries (PAs) is important to the evaluation of pulmonary vascular function. Early and current efforts have focused on the arteries' histological changes, their mechanical properties under in vitro mechanical testing, and their zero-stress and no-load states. However, the linkage between the histology and mechanical behavior is still not well understood. To explore this linkage, we investigated the geometry, residual stretch, and histology of proximal PAs in both adult rat and neonatal calf hypoxic models of pulmonary hypertension (PH), compared their changes due to chronic hypoxia across species, and proposed a two-layer mechanical model of artery to relate the opening angle to the stiffness ratio of the PA outer to inner layer. We found that the proximal PA remodeling in calves was quite different from that in rats. In rats, the arterial wall thickness, inner diameter, and outer layer thickness fraction all increased dramatically in PH and the opening angle decreased significantly, whereas in calves, only the arterial wall thickness increased in PH. The proposed model predicted that the stiffness ratio of the calf proximal PAs changed very little from control to hypertensive group, while the decrease of opening angle in rat proximal PAs in response to chronic hypoxia was approximately linear to the increase of the stiffness ratio. We conclude that the arterial remodeling in rat and calf proximal PAs is different and the change of opening angle can be linked to the change of the arterial histological structure and mechanics.

Increased carotid arterial wall thickness in common hyperlipidemia

1995 ◽  
Vol 6 (1) ◽  
pp. 57-64 ◽  
Author(s):  
Agostino Gnasso ◽  
Arturo Pujia ◽  
Concetta Irace ◽  
Pier Luigi Mattioli
Keyword(s):  
Wall Thickness ◽  
Arterial Wall ◽  
Arterial Wall Thickness ◽  
Carotid Arterial

Reproducibility of Ultrasonographically Determined Intima-Media Thickness Is Dependent on Arterial Wall Thickness

Stroke ◽  
1997 ◽  
Vol 28 (10) ◽  
pp. 1972-1980 ◽  
Author(s):  
Eva Stensland-Bugge ◽  
Kaare H. Bønaa ◽  
Oddmund Joakimsen
Keyword(s):  
Wall Thickness ◽  
Arterial Wall ◽  
Intima Media Thickness ◽  
Arterial Wall Thickness ◽  
Media Thickness

scholarly journals Clinical and vascular responses to propranolol and candesartan in migraine patients: A randomized controlled clinical trial

2020 ◽  
Vol 3 ◽  
pp. 251581632094649
Author(s):  
Aros Dlawer Barzenje ◽  
Knut Gjesdal ◽  
Bendik Slagsvold Winsvold ◽  
Milada Cvancarova Småstuen ◽  
Lars Jacob Stovner ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Arterial Wall ◽  
Clinical Effect ◽  
Arterial Compliance ◽  
Drug Effects ◽  
Controlled Clinical Trial ◽  
Noninvasive Blood Pressure ◽  
Randomized Controlled ◽  
Prophylactic Drugs ◽  
Wall Stiffness

Background: Both propranolol and candesartan are prophylactic drugs for migraine, but with unknown mechanisms of action. The objectives of the present study were to investigate these drugs’ effects on arterial wall dynamics and the potential relation between their vascular and clinical effect. Methods: The study was based on data from a previously published randomized, placebo-controlled, triple-blinded, double crossover clinical trial comparing the prophylactic effects of candesartan and propranolol in 72 patients. Finapres noninvasive blood pressure curves were analyzed. On the descending limb of the pulse curve, a notch is produced by pulse wave reflection, and its relative height compared to the top of the curve (the notch ratio) was used as a marker of arterial wall stiffness. Results: Candesartan decreased the notch ratio from baseline ( p = 0.005), reflecting more compliant arteries and vasodilation, whereas propranolol increased the notch ratio ( p = 0.005), reflecting less compliant arteries and vasoconstriction. There was no difference in baseline notch ratio between clinical responders and nonresponders. Conclusion: The drugs are both efficient prophylactic medications, yet they have opposite effects on arterial wall dynamics. This suggests that drug effects other than those on arterial compliance must be responsible for their prophylactic effect in migraine.

Gender difference in the influence of smoking on arterial wall thickness

2000 ◽  
Vol 153 (1) ◽  
pp. 139-145 ◽  
Author(s):  
Jérôme Gariepy ◽  
Nicolas Denarie ◽  
Gilles Chironi ◽  
Jean Salomon ◽  
Jaime Levenson ◽  
...  
Keyword(s):  
Gender Difference ◽  
Wall Thickness ◽  
Arterial Wall ◽  
Arterial Wall Thickness
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