scholarly journals Hemodynamic force triggers rapid NETosis within sterile thrombotic occlusions

2018 ◽  
Vol 16 (2) ◽  
pp. 316-329 ◽  
Author(s):  
X. Yu ◽  
J. Tan ◽  
S. L. Diamond
Keyword(s):  
Hemodynamic Force

Hemodynamic-Force-Induced Difference of Interendothelial Junctional Complexesa

2006 ◽  
Vol 748 (1) ◽  
pp. 104-120 ◽  
Author(s):  
YOJI YOSHIDA ◽  
MITSUJI OKANO ◽  
SU WANG ◽  
MASAHIRO KOBAYASHI ◽  
MASAHIKO KAWASUMI ◽  
...  
Keyword(s):  
Hemodynamic Force

Role of Rheological Parameters in Blood-Endothelial Nano-Scale Interactions

2010 ◽  
Author(s):  
Abdullah A. Alshorman
Keyword(s):  
Shear Rate ◽  
Blood Viscosity ◽  
Simulation Analysis ◽  
Rheological Parameters ◽  
Surface Shear ◽  
Characteristic Structure ◽  
Rolling Velocity ◽  
Cell Rolling ◽  
Nano Scale ◽  
Hemodynamic Force

The performance of endothelium layer under the effect of blood shear force depends fundamentally on the rheological parameters of the blood flow, characteristic structure and physiological response of this lining layer to the shear effect. This includes the nano-scale geometry of blood cells and endothelium surface, shear rate and blood viscosity, in addition to endothelial mechanical properties. Principally, the elucidation of these nanoscale interactions will contribute the explanation and better understanding of cardiovascular diseases that are the main causes of death and health suffering for millions of people all over the world. As an attempt to build up a tangible contribution for this revelation, a simulation analysis has been performed to study the effects of blood shear stress and blood dynamic viscosity on the rate of attachment and detachment of blood over the endothelium layer in the form of adhesion and rolling. In particular, the nature of each effect has been determined and the numerical ranges for each parameter have been estimated for the physiological range of shear rates. The results reveal that shear rate G enhances the blood cell rolling starting from 20 s−1 up to 90 s−1 then it tends to have constant contribution regardless its value ever greater than 90 s−1. Likewise, higher and moderate blood viscosity μ (i.e., 0.5–2.5 cP) supports rolling up to 4 cP, then it starts to keep its influence constant similar to that of shear rate. However, lower μ enhances the enhances the steady rolling at low rolling velocity, which open a room for primary and/or permanent adhesion. The rolling starts at μ = 0.0.5 cP, then jumped to higher values when μ was increased. The effect of μ on rolling is similar to that of shear rate because of their jointed role in the hemodynamic force, such that the increase of both of them drives the cell for faster rolling up to maximum limit, then discontinue affecting. Fundamentally, the most effective biophysiological range of μ on cell rolling is 0.1–3.0 cP, which is suggested by this study and mainly used in the previous investigations. However, the most frequent used rang of μ was 1–2 cP.

2C36 Hemodynamic force is a physical regulator of heart development

2014 ◽  
Vol 2014.26 (0) ◽  
pp. 373
Author(s):  
Toshihiro BANJO ◽  
Daisuke YOSHINO ◽  
Kota MIYASAKA ◽  
Yasuyuki KIDA ◽  
Masaaki SATO ◽  
...  
Keyword(s):  
Heart Development ◽  
Hemodynamic Force

Microarray profiling revealsCXCR4ais downregulated by blood flow in vivo and mediates collateral formation in zebrafish embryos

2009 ◽  
Vol 38 (3) ◽  
pp. 319-327 ◽  
Author(s):  
Ian M. Packham ◽  
Caroline Gray ◽  
Paul R. Heath ◽  
Paul G. Hellewell ◽  
Philip W. Ingham ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Contraction ◽  
Zebrafish Embryos ◽  
Knock Down ◽  
Transcriptional Effect ◽  
Vessel Development ◽  
Hemodynamic Force ◽  
Collateral Vessels ◽  
And Control

The response to hemodynamic force is implicated in a number of pathologies including collateral vessel development. However, the transcriptional effect of hemodynamic force is extremely challenging to examine in vivo in mammals without also detecting confounding processes such as hypoxia and ischemia. We therefore serially examined the transcriptional effect of preventing cardiac contraction in zebrafish embryos which can be deprived of circulation without experiencing hypoxia since they obtain sufficient oxygenation by diffusion. Morpholino antisense knock-down of cardiac troponin T2 ( tnnt2) prevented cardiac contraction without affecting vascular development. Gene expression in whole embryo RNA from tnnt2 or control morphants at 36, 48, and 60 h postfertilization (hpf) was assessed using Affymetrix GeneChip Zebrafish Genome Arrays (>14,900 transcripts). We identified 308 differentially expressed genes between tnnt2 and control morphants. One such ( CXCR4a) was significantly more highly expressed in tnnt2 morphants at 48 and 60 hpf than controls. In situ hybridization localized CXCR4a upregulation to endothelium of both tnnt2 morphants and gridlock mutants (which have an occluded aorta preventing distal blood flow). This upregulation appears to be of functional significance as either CXCR4a knock-down or pharmacologic inhibition impaired the ability of gridlock mutants to recover blood flow via collateral vessels. We conclude absence of hemodynamic force induces endothelial CXCR4a upregulation that promotes recovery of blood flow.

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