scholarly journals In Vitro Measurement of Blood Flow in Microvascular Network with Realistic Geometry

2019 ◽  
Vol 16 (S2) ◽  
pp. 38-39
Author(s):  
Ken-ichi Tsubota ◽  
Yuya Kodama ◽  
Hiroyoshi Aoki ◽  
Yutaka Yamagata
2019 ◽  
Vol 88 ◽  
pp. 88-94 ◽  
Author(s):  
Yuya Kodama ◽  
Hiroyoshi Aoki ◽  
Yutaka Yamagata ◽  
K. Tsubota

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S198-S198
Author(s):  
Joseph R Meno ◽  
Thien-son K Nguyen ◽  
Elise M Jensen ◽  
G Alexander West ◽  
Leonid Groysman ◽  
...  

1984 ◽  
Vol 52 (02) ◽  
pp. 102-104 ◽  
Author(s):  
L J Nicholson ◽  
J M F Clarke ◽  
R M Pittilo ◽  
S J Machin ◽  
N Woolf

SummaryA technique for harvesting mesothelial cells is described. This entails collagenase digestion of omentum after which the cells can be cultured. The technique has been developed using the rat, but has also been successfully applied to human tissue. Cultured rat mesothelial cells obtained in this way have been examined by scanning electron microscopy. Rat mesothelial cells grown on plastic film have been exposed to blood in an in vitro system using a Baumgartner chamber and have been demonstrated to support blood flow. No adhering platelets were observed on the mesothelial cell surface. Fibroblasts similarily exposed to blood as a control were washed off the plastic.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Gautier Follain ◽  
Naël Osmani ◽  
Valentin Gensbittel ◽  
Nandini Asokan ◽  
Annabel Larnicol ◽  
...  

AbstractTumor progression and metastatic dissemination are driven by cell-intrinsic and biomechanical cues that favor the growth of life-threatening secondary tumors. We recently identified pro-metastatic vascular regions with blood flow profiles that are permissive for the arrest of circulating tumor cells. We have further established that such flow profiles also control endothelial remodeling, which favors extravasation of arrested CTCs. Yet, how shear forces control endothelial remodeling is unknown. In the present work, we aimed at dissecting the cellular and molecular mechanisms driving blood flow-dependent endothelial remodeling. Transcriptomic analysis of endothelial cells revealed that blood flow enhanced VEGFR signaling, among others. Using a combination of in vitro microfluidics and intravital imaging in zebrafish embryos, we now demonstrate that the early flow-driven endothelial response can be prevented upon specific inhibition of VEGFR tyrosine kinase and subsequent signaling. Inhibitory targeting of VEGFRs reduced endothelial remodeling and subsequent metastatic extravasation. These results confirm the importance of VEGFR-dependent endothelial remodeling as a driving force of CTC extravasation and metastatic dissemination. Furthermore, the present work suggests that therapies targeting endothelial remodeling might be a relevant clinical strategy in order to impede metastatic progression.


2021 ◽  
Vol 18 (2) ◽  
pp. 147916412199903
Author(s):  
Laura Croteau ◽  
Clément Mercier ◽  
Étienne Fafard-Couture ◽  
Alexandre Nadeau ◽  
Stéphanie Robillard ◽  
...  

Aims: Peripheral artery disease is a complication of diabetes leading to critical hindlimb ischemia. Diabetes-induced inhibition of VEGF actions is associated with the activation of protein kinase Cδ (PKCδ). We aim to specifically investigate the role of PKCδ in endothelial cell (EC) function and VEGF signaling. Methods: Nondiabetic and diabetic mice, with ( ec-Prkcd−/−) or without ( ec-Prkcdf/f) endothelial deletion of PKCδ, underwent femoral artery ligation. Blood flow reperfusion was assessed up to 4 weeks post-surgery. Capillary density, EC apoptosis and VEGF signaling were evaluated in the ischemic muscle. Src homology region 2 domain-containing phosphatase-1 (SHP-1) phosphatase activity was assessed in vitro using primary ECs. Results: Ischemic muscle of diabetic ec-Prkcdf/f mice exhibited reduced blood flow reperfusion and capillary density while apoptosis increased as compared to nondiabetic ec-Prkcdf/f mice. In contrast, blood flow reperfusion and capillary density were significantly improved in diabetic ec-Prkcd−/− mice. VEGF signaling pathway was restored in diabetic ec-Prkcd−/− mice. The deletion of PKCδ in ECs prevented diabetes-induced VEGF unresponsiveness through a reduction of SHP-1 phosphatase activity. Conclusions: Our data provide new highlights in mechanisms by which PKCδ activation in EC contributed to poor collateral vessel formation, thus, offering novel therapeutic targets to improve angiogenesis in the diabetic limb.


2021 ◽  
pp. 039139882110130
Author(s):  
Guang-Mao Liu ◽  
Fu-Qing Jiang ◽  
Xiao-Han Yang ◽  
Run-Jie Wei ◽  
Sheng-Shou Hu

Blood flow inside the left ventricle (LV) is a concern for blood pump use and contributes to ventricle suction and thromboembolic events. However, few studies have examined blood flow inside the LV after a blood pump was implanted. In this study, in vitro experiments were conducted to emulate the intraventricular blood flow, such as blood flow velocity, the distribution of streamlines, vorticity and the standard deviation of velocity inside the LV during axial blood pump support. A silicone LV reconstructed from computerized tomography (CT) data of a heart failure patient was incorporated into a mock circulatory loop (MCL) to simulate human systemic circulation. Then, the blood flow inside the ventricle was examined by particle image velocimetry (PIV) equipment. The results showed that the operating conditions of the axial blood pump influenced flow patterns within the LV and areas of potential blood stasis, and the intraventricular swirling flow was altered with blood pump support. The presence of vorticity in the LV from the thoracic aorta to the heart apex can provide thorough washing of the LV cavity. The gradually extending stasis region in the central LV with increasing blood pump support is necessary to reduce the thrombosis potential in the LV.


2021 ◽  
Vol 117 ◽  
pp. 110241
Author(s):  
Alberto Coccarelli ◽  
Supratim Saha ◽  
Tanjeri Purushotham ◽  
K. Arul Prakash ◽  
Perumal Nithiarasu

1984 ◽  
Vol 246 (2) ◽  
pp. G195-G203
Author(s):  
R. H. Gallavan ◽  
Y. Tsuchiya ◽  
E. D. Jacobson

The purpose of this study was to determine the effects of nicotine on intestinal blood flow and oxygen consumption. The intravenous infusion of nicotine at doses corresponding to those experienced by smokers produced a transient increase in systemic arterial blood pressure and mesenteric blood flow. Subsequently a steady-state response developed that consisted of a reduction in mesenteric blood flow due to both a decrease in blood pressure and an increase in intestinal vascular resistance. This increase in resistance was probably due to increased levels of circulating catecholamines. The intra-arterial infusion of nicotine into the intestinal circulation at doses experienced by the average smoker had no effect on either intestinal blood flow or oxygen consumption. Similarly, under in vitro conditions nicotine had no direct effect on intestinal vascular smooth muscle tension. Thus, nicotine appears to reduce intestinal blood flow indirectly as a result of its systemic effects.


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