scholarly journals Shear stress‐induced flow‐mediated dilatation: is it up to haemoglobin?

2020 ◽  
Vol 598 (24) ◽  
pp. 5609-5610
Author(s):  
Andrew Oneglia ◽  
Sauyeh Zamani ◽  
Miles F. Bartlett
2008 ◽  
Vol 105 (2) ◽  
pp. 427-432 ◽  
Author(s):  
Mandeep Dhindsa ◽  
Shawn M. Sommerlad ◽  
Allison E. DeVan ◽  
Jill N. Barnes ◽  
Jun Sugawara ◽  
...  

The clinical importance of vascular reactivity as an early marker of atherosclerosis has been well established, and a number of established and emerging techniques have been employed to provide measurements of peripheral vascular reactivity. However, relations between these methodologies are unclear as each technique evaluates different physiological aspects related to micro- and macrovascular reactive hyperemia. To address this question, a total of 40 apparently healthy normotensive adults, 19–68 yr old, underwent 5 min of forearm suprasystolic cuff-induced ischemia followed by postischemic measurements. Measurements of vascular reactivity included 1) flow-mediated dilatation (FMD), 2) changes in pulse wave velocity between the brachial and radial artery (ΔPWV), 3) hyperemic shear stress, 4) reactive hyperemic flow, 5) reactive hyperemia index (RHI) assessed by fingertip arterial tonometry, 6) fingertip temperature rebound (TR), and 7) skin reactive hyperemia. FMD was significantly and positively associated with RHI ( r = 0.47) and TR ( r = 0.45) (both P < 0.01) but not with reactive hyperemic flow or hyperemic shear stress. There was no correlation between two measures of macrovascular reactivity (FMD and ΔPWV). Skin reactive hyperemia was significantly associated with RHI ( r = 0.55) and reactive hyperemic flow ( r = 0.35) (both P < 0.05). There was a significant association between reactive hyperemia and RHI ( r = 0.30; P < 0.05). In more than 75% of cases, vascular reactivity measures were not significantly associated. We concluded that associations among different measures of peripheral micro- and macrovascular reactivity were modest at best. These results suggest that different physiological mechanisms may be involved in changing different measures of vascular reactivity.


2008 ◽  
Vol 13 (4) ◽  
pp. 263-270 ◽  
Author(s):  
Lawrence M Title ◽  
Evan Lonn ◽  
Francois Charbonneau ◽  
Marinda Fung ◽  
Kieren J Mather ◽  
...  

Author(s):  
Holden W. Hemingway ◽  
Rauchelle E. Richey ◽  
Amy M. Moore ◽  
Austin M. Shokraeifard ◽  
Gabriel C. Thomas ◽  
...  

Acute heat exposure protects against endothelial ischemia-reperfusion (I/R) injury in humans. However, the mechanism/s mediating this protective effect remain unclear. We tested the hypothesis that inhibiting the increase in shear stress induced by acute heat exposure would attenuate the protection of endothelial function following I/R injury. Nine (3 women) young healthy participants were studied under 3 experimental conditions: 1) thermoneutral control; 2) whole-body heat exposure to increase body core temperature by 1.2 °C; 3) heat exposure + brachial artery compression to inhibit the temperature-dependent increase in shear stress. Endothelial function was assessed via brachial artery flow-mediated dilatation before (pre-I/R) and after (post-I/R) 20 min of arm ischemia followed by 20 min of reperfusion. Brachial artery shear rate was increased during heat exposure (681 ± 359 s-1), but not for thermoneutral control (140 ± 63 s-1; P < 0.01 vs. heat exposure) nor heat + brachial artery compression (139 ± 60 s-1; P < 0.01 vs. heat exposure). Ischemia-reperfusion injury reduced flow-mediated dilatation following thermoneutral control (pre-I/R, 5.5 ± 2.9 % vs. post-I/R, 3.8 ± 2.9 %; P = 0.06), but was protected following heat exposure (pre-I/R, 5.8 ± 2.9 % vs. post-I/R, 6.1 ± 2.9 %; P = 0.5) and heat + arterial compression (pre-I/R, 4.4 ± 2.8 % vs. post-I/R, 5.8 ± 2.8 %; P = 0.1). Contrary to our hypothesis, our findings demonstrate that shear stress induced by acute heat exposure is not obligatory to protect against endothelial I/R injury in humans.


2013 ◽  
Vol 14 (1-2) ◽  
pp. 109-115
Author(s):  
Michael Stiehm ◽  
Martin Brede ◽  
Daniel Quosdorf ◽  
Alfred Leder

AbstractThe post-operative situation in a stented vessel is characterised by struts which extend into the vessel lumen. These barriers on the surface provoke a topological change of the blood flow inducing flow deceleration and stagnation zones. Low values of wall shear stress (WSS) especially up- and downstream of the struts are found accordingly. Clinical studies correlate the occurrence of complications like restenosis and thrombosis with the alteration of the spatial WSS distribution. In this study 3D computational models were used to characterise the flow topology of three different stent types. For this purpose steady state simulations of the flow field within a simplified stented coronary artery were performed. The stent types differ in their strut patterns so that the variation of the induced flow structures can be observed. The aim of these investigations is to evaluate the effect of a purposeful flow control by altering the design of the struts. An improved alignment of the struts will be able to guide the flow to benefit the spatial WSS distribution. To compare the performance of the different stent types the size of the area charged with a WSS value below 0.5 Pa is used as a criterion. We will demonstrate that those strut pattern which generate helical flow structures significantly reduce the critical region of low WSS values.


Author(s):  
Jeong-Min Lee ◽  
Yi-Seul Jo ◽  
Sung-Min Kim ◽  
Youn-Jea Kim

In this study, the flow characteristics of the Coandă nozzle were studied with various values of the aspect ratio of induced flow inlet to outlet. Furthermore, four different applied pressure conditions of compressed air were also considered. Numerical analysis was performed using the commercial CFD code, ANSYS CFX with a shear stress transport (SST) turbulent model. The results of total pressure and velocity distributions were graphically depicted with various geometrical configurations and operating conditions.


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