scholarly journals Rôle of contrast media viscosity in altering vessel wall shear stress and relation to the risk of contrast extravasations

2016 ◽  
Vol 38 (12) ◽  
pp. 1426-1433 ◽  
Author(s):  
Sophia Sakellariou ◽  
Wenguang Li ◽  
Manosh C Paul ◽  
Giles Roditi
2019 ◽  
Vol 316 (1) ◽  
pp. C92-C103 ◽  
Author(s):  
Hojin Kang ◽  
Zhigang Hong ◽  
Ming Zhong ◽  
Jennifer Klomp ◽  
Kayla J. Bayless ◽  
...  

Angiogenesis is initiated in response to a variety of external cues, including mechanical and biochemical stimuli; however, the underlying signaling mechanisms remain unclear. Here, we investigated the proangiogenic role of the endothelial mechanosensor Piezo1. Genetic deletion and pharmacological inhibition of Piezo1 reduced endothelial sprouting and lumen formation induced by wall shear stress and proangiogenic mediator sphingosine 1-phosphate, whereas Piezo1 activation by selective Piezo1 activator Yoda1 enhanced sprouting angiogenesis. Similarly to wall shear stress, sphingosine 1-phosphate functioned by activating the Ca2+ gating function of Piezo1, which in turn signaled the activation of the matrix metalloproteinase-2 and membrane type 1 matrix metalloproteinase during sprouting angiogenesis. Studies in mice in which Piezo1 was conditionally deleted in endothelial cells demonstrated the requisite role of sphingosine 1-phosphate-dependent activation of Piezo1 in mediating angiogenesis in vivo. These results taken together suggest that both mechanical and biochemical stimuli trigger Piezo1-mediated Ca2+ influx and thereby activate matrix metalloproteinase-2 and membrane type 1 matrix metalloproteinase and synergistically facilitate sprouting angiogenesis.


2015 ◽  
Vol 5 (1) ◽  
pp. 90-100 ◽  
Author(s):  
Vitaly Kheyfets ◽  
Mirunalini Thirugnanasambandam ◽  
Lourdes Rios ◽  
Daniel Evans ◽  
Triston Smith ◽  
...  

1996 ◽  
pp. 403-407 ◽  
Author(s):  
Moreno Bardelli ◽  
Renzo Carretta ◽  
Domenico Dotti ◽  
Bruno Fabris ◽  
Fabio Fischetti ◽  
...  

Author(s):  
Hui Meng ◽  
Sabareesh K. Natarajan ◽  
Eleni Metaxa ◽  
Markus Tremmel ◽  
Ling Gao ◽  
...  

Hemodynamic insult has long been speculated to be a key factor in intracranial aneurysm (IA) formation,1 but the specifics of hemodynamic insult contributing to this process are not understood. Despite other risk factors, IAs are predominantly found at locations associated with unique hemodynamic stress such as at the apices of arterial bifurcations or outer curves, prominent in high wall shear stress (WSS) and wall shear stress gradients (WSSG).2 Furthermore, it appears that increased flow at these locations is required to trigger the initiation of aneurysmal remodeling.3 We have previously shown that increasing flow in the rabbit basilar artery (BA), secondary to common carotid artery (CCA) ligation, resulted in nascent aneurysm development at the basilar terminus (BT).4 However, it is unclear if certain hemodynamic stress thresholds must be exceeded to trigger aneurysmal remodeling, and whether sustained insult is necessary.


Author(s):  
Jennifer Dolan ◽  
Song Liu ◽  
Hui Meng ◽  
John Kolega

In both human and animal models, cerebral aneurysms tend to develop at the apices of bifurcations in the cerebral vasculature. Due to the focal nature of aneurysm development it has long been speculated that hemodynamics are an important factor in aneurysm susceptibility. The local hemodynamics of bifurcations are complex, being characterized by flow impingement causing a high frictional force on the vessel wall known as wall shear stress (WSS) and significant flow acceleration or deceleration, manifested as the positive or negative spatial gradient of WSS (WSSG). In vivo studies have recently identified that aneurysm initiation occurs at areas of the vessel wall that experience a combination of both high WSS and positive WSSG [1,2]


2011 ◽  
Vol 32 (3) ◽  
pp. 587-594 ◽  
Author(s):  
Z. Kulcsár ◽  
Á. Ugron ◽  
M. Marosfői ◽  
Z. Berentei ◽  
G. Paál ◽  
...  

2011 ◽  
Vol 301 (6) ◽  
pp. H2254-H2263 ◽  
Author(s):  
Henry Y. Chen ◽  
Anjan K. Sinha ◽  
Jenny S. Choy ◽  
Hai Zheng ◽  
Michael Sturek ◽  
...  

Stent can cause flow disturbances on the endothelium and compliance mismatch and increased stress on the vessel wall. These effects can cause low wall shear stress (WSS), high wall shear stress gradient (WSSG), oscillatory shear index (OSI), and circumferential wall stress (CWS), which may promote neointimal hyperplasia (IH). The hypothesis is that stent-induced abnormal fluid and solid mechanics contribute to IH. To vary the range of WSS, WSSG, OSI, and CWS, we intentionally mismatched the size of stents to that of the vessel lumen. Stents were implanted in coronary arteries of 10 swine. Intravascular ultrasound (IVUS) was used to size the coronary arteries and stents. After 4 wk of stent implantation, IVUS was performed again to determine the extent of IH. In conjunction, computational models of actual stents, the artery, and non-Newtonian blood were created in a computer simulation to yield the distribution of WSS, WSSG, OSI, and CWS in the stented vessel wall. An inverse relation ( R2 = 0.59, P < 0.005) between WSS and IH was found based on a linear regression analysis. Linear relations between WSSG, OSI, and IH were observed ( R2 = 0.48 and 0.50, respectively, P < 0.005). A linear relation ( R2 = 0.58, P < 0.005) between CWS and IH was also found. More statistically significant linear relations between the ratio of CWS to WSS (CWS/WSS), the products CWS × WSSG and CWS × OSI, and IH were observed ( R2 = 0.67, 0.54, and 0.56, respectively, P < 0.005), suggesting that both fluid and solid mechanics influence the extent of IH. Stents create endothelial flow disturbances and intramural wall stress concentrations, which correlate with the extent of IH formation, and these effects were exaggerated with mismatch of stent/vessel size. These findings reveal the importance of reliable vessel and stent sizing to improve the mechanics on the vessel wall and minimize IH.


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