Electrochemical Surface Shear Rate Evaluation in Models of the Renal Artery

1982 ◽  
Vol 104 (4) ◽  
pp. 290-295 ◽  
Author(s):  
O. A. El Masry ◽  
I. A. Feuerstein
Keyword(s):  
Shear Rate ◽  
Renal Artery ◽  
Surface Shear ◽  
Atherosclerotic Lesions ◽  
Shape Influence ◽  
Rate Evaluation ◽  
Mathematical Relationships ◽  
Flow Division ◽  
Parent Tube

Electrochemical measurements of surface shear rate were done in two renal artery models with 45 and 90-deg take-off angles to determine the extent to which the parent tube flow rate, flow division and branch shape influence flow at sites for atherogenesis. The dependence of surface shear rate on each of these independent variables was nonlinear; mathematical relationships which could predict surface shear rate at other flow rates, flow divison ratios or vessel shapes did not emerge. The results of this work along with reports of others, which demonstrate great variability in location and extent of atherosclerotic lesions, support the conclusion that pathological studies and flow studies should be done simultaneously if the role of flow in atherogenesis is to be elucidated.

Platelet and Shear Rate Promote Tumor Cell Adhesion to Human Endothelial Extracellular Matrix - Absence of a Role for Platelet Cyclooxygenase

1989 ◽  
Vol 61 (03) ◽  
pp. 485-489 ◽  
Author(s):  
Eva Bastida ◽  
Lourdes Almirall ◽  
Antonio Ordinas
Keyword(s):  
Cell Adhesion ◽  
Shear Rate ◽  
Tumor Cell ◽  
Umbilical Vein ◽  
Blood Platelets ◽  
Flow Conditions ◽  
Tumor Cell Adhesion ◽  
Rate Dependent ◽  
Static Conditions

SummaryBlood platelets are thought to be involved in certain aspects of malignant dissemination. To study the role of platelets in tumor cell adherence to vascular endothelium we performed studies under static and flow conditions, measuring tumor cell adhesion in the absence or presence of platelets. We used highly metastatic human adenocarcinoma cells of the lung, cultured human umbilical vein endothelial cells (ECs) and extracellular matrices (ECM) prepared from confluent EC monolayers. Our results indicated that under static conditions platelets do not significantly increase tumor cell adhesion to either intact ECs or to exposed ECM. Conversely, the studies performed under flow conditions using the flat chamber perfusion system indicated that the presence of 2 × 105 pl/μl in the perfusate significantly increased the number of tumor cells adhered to ECM, and that this effect was shear rate dependent. The maximal values of tumor cell adhesion were obtained, in presence of platelets, at a shear rate of 1,300 sec-1. Furthermore, our results with ASA-treated platelets suggest that the role of platelets in enhancing tumor cell adhesion to ECM is independent of the activation of the platelet cyclooxygenase pathway.

scholarly journals Pentraxin 3: A Novel Biomarker for Inflammatory Cardiovascular Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Kenji Inoue ◽  
Tatsuhiko Kodama ◽  
Hiroyuki Daida
Keyword(s):  
Gene Expression ◽  
Cardiovascular Disease ◽  
Pentraxin 3 ◽  
Human Endothelial Cells ◽  
C Reactive Protein ◽  
Physiological Concentration ◽  
Reactive Protein ◽  
Atherosclerotic Lesions ◽  
Human Genes

Numerous studies have recently examined the role of pentraxin 3 (PTX3) in clinical situations. The pentraxin family includes C-reactive protein (CRP); however, unlike CRP, PTX3 is expressed predominantly in atherosclerotic lesions that involve macrophages, neutrophils, dendritic cells, or smooth muscle cells. Interestingly, PTX3 gene expression in human endothelial cells is suppressed to a greater extent by pitavastatin than the expression of 6,000 other human genes that have been examined, suggesting that PTX3 may be a novel biomarker for inflammatory cardiovascular disease. The expression and involvement of PTX3 in cardiovascular diseases are discussed in this paper, along with the characteristics of PTX3 that make it a suitable biomarker; namely, that the physiological concentration is known and it is independent of other risk factors. The results discussed in this paper suggest that further investigations into the potential novel use of PTX3 as a biomarker for inflammatory cardiovascular disease should be undertaken.

The role of elasticity in thixotropy: Transient elastic stress during stepwise reduction in shear rate

2021 ◽  
Vol 33 (3) ◽  
pp. 033112
Author(s):  
Jiho Choi ◽  
Matthew Armstrong ◽  
Simon A. Rogers
Keyword(s):  
Shear Rate ◽  
Elastic Stress ◽  
Stepwise Reduction

scholarly journals The role of proteoglycan (versican) cleavage by the metalioenzyme matrilysin in unstable atherosclerotic lesions in patients

1996 ◽  
Vol 27 (2) ◽  
pp. 355-356 ◽  
Author(s):  
Igor Halpert ◽  
Samuel A. Wickline ◽  
Jill D. Roby ◽  
Ulrike D. Sires ◽  
Thomas N. Wright ◽  
...  
Keyword(s):  
Atherosclerotic Lesions

scholarly journals Importance of Primary Capture and L-Selectin–Dependent Secondary Capture in Leukocyte Accumulation in Inflammation and Atherosclerosis in Vivo

2001 ◽  
Vol 194 (2) ◽  
pp. 205-218 ◽  
Author(s):  
Einar E. Eriksson ◽  
Xun Xie ◽  
Joachim Werr ◽  
Peter Thoren ◽  
Lennart Lindbom
Keyword(s):  
Shear Rate ◽  
Leukocyte Recruitment ◽  
Wall Shear Rate ◽  
Free Flow ◽  
Initial Contact ◽  
Atherosclerotic Lesions ◽  
Leukocyte Accumulation ◽  
Wall Shear ◽  
Rolling Leukocytes

In the multistep process of leukocyte extravasation, the mechanisms by which leukocytes establish the initial contact with the endothelium are unclear. In parallel, there is a controversy regarding the role for L-selectin in leukocyte recruitment. Here, using intravital microscopy in the mouse, we investigated leukocyte capture from the free flow directly to the endothelium (primary capture), and capture mediated through interactions with rolling leukocytes (secondary capture) in venules, in cytokine-stimulated arterial vessels, and on atherosclerotic lesions in the aorta. Capture was more prominent in arterial vessels compared with venules. In venules, the incidence of capture increased with increasing vessel diameter and wall shear rate. Secondary capture required a minimum rolling leukocyte flux and contributed by ∼20–50% of total capture in all studied vessel types. In arteries, secondary capture induced formation of clusters and strings of rolling leukocytes. Function inhibition of L-selectin blocked secondary capture and thereby decreased the flux of rolling leukocytes in arterial vessels and in large (>45 μm in diameter), but not small (<45 μm), venules. These findings demonstrate the importance of leukocyte capture from the free flow in vivo. The different impact of blockage of secondary capture in venules of distinct diameter range, rolling flux, and wall shear rate provides explanations for the controversy regarding the role of L-selectin in various situations of leukocyte recruitment. What is more, secondary capture occurs on atherosclerotic lesions, a fact that provides the first evidence for roles of L-selectin in leukocyte accumulation in atherogenesis.

Role of EP2 and EP3 PGE2receptors in control of murine renal hemodynamics

2001 ◽  
Vol 280 (1) ◽  
pp. H327-H333 ◽  
Author(s):  
Laurent P. Audoly ◽  
Xiaoping Ruan ◽  
Victoria A. Wagner ◽  
Jennifer L. Goulet ◽  
Stephen L. Tilley ◽  
...  
Keyword(s):  
Renal Artery ◽  
Vascular Reactivity ◽  
Renal Hemodynamics ◽  
Receptor Subtypes ◽  
Male Mice ◽  
Unique Role ◽  
Arterial Blood ◽  
Renal Vascular

The kidney plays a central role in long-term regulation of arterial blood pressure and salt and water homeostasis. This is achieved in part by the local actions of paracrine and autacoid mediators such as the arachidonic acid-prostanoid system. The present study tested the role of specific PGE2 E-prostanoid (EP) receptors in the regulation of renal hemodynamics and vascular reactivity to PGE2. Specifically, we determined the extent to which the EP2 and EP3 receptor subtypes mediate the actions of PGE2 on renal vascular tone. Renal blood flow (RBF) was measured by ultrasonic flowmetry, whereas vasoactive agents were injected directly into the renal artery of male mice. Studies were performed on two independent mouse lines lacking either EP2or EP3 (−/−) receptors and the results were compared with wild-type controls (+/+). Our results do not support a unique role of the EP2 receptor in regulating overall renal hemodynamics. Baseline renal hemodynamics in EP2−/− mice [RBF EP2−/−: 5.3 ± 0.8 ml · min−1 · 100 g kidney wt−1; renal vascular resistance (RVR) 19.7 ± 3.6 mmHg · ml−1 · min · g kidney wt] did not differ statistically from control mice (RBF +/+: 4.0 ± 0.5 ml · min−1 · 100 g kidney wt−1; RVR +/+: 25.4 ± 4.9 mmHg · ml−1 · min · 100 g kidney wt−1). This was also the case for the peak RBF increase after local PGE2 (500 ng) injection into the renal artery (EP2−/−: 116 ± 4 vs. +/+: 112 ± 2% baseline RBF). In contrast, we found that the absence of EP3receptors in EP3−/− mice caused a significant increase (43%) in basal RBF (7.9 ± 0.8 ml · min−1 · g kidney wt−1, P < 0.05 vs. +/+) and a significant decrease (41%) in resting RVR (11.6 ± 1.4 mmHg · ml−1 · min · g kidney wt−1, P < 0.05 vs. +/+). Local administration of 500 ng of PGE2 into the renal artery caused more pronounced renal vasodilation in EP3−/− mice (128 ± 2% of basal RBF, P < 0.05 vs. +/+). We conclude that EP3 receptors mediate vasoconstriction in the kidney of male mice and its actions are tonically active in the basal state. Furthermore, EP3receptors are capable of buffering PGE2-mediated renal vasodilation.

scholarly journals Platelet von Willebrand factor: evidence for its involvement in platelet adhesion to collagen

Blood ◽  
1987 ◽  
Vol 70 (4) ◽  
pp. 1214-1217
Author(s):  
E Fressinaud ◽  
D Baruch ◽  
C Rothschild ◽  
HR Baumgartner ◽  
D Meyer
Keyword(s):  
Shear Rate ◽  
Von Willebrand Factor ◽  
Platelet Adhesion ◽  
Von Willebrand Disease ◽  
High Shear ◽  
Shear Rates ◽  
High Shear Rates ◽  
Von Willebrand ◽  
Willebrand Factor

Although it is well established that plasma von Willebrand Factor (vWF) is essential to platelet adhesion to subendothelium at high shear rates, the role of platelet vWF is less clear. We studied the respective role of both plasma and platelet vWF in mediating platelet adhesion to fibrillar collagen in a parallel-plate perfusion chamber. Reconstituted blood containing RBCs, various mixtures of labeled washed platelets and plasma from controls or five patients with severe von Willebrand disease (vWD), was perfused through the chamber for five minutes at a shear rate of 1,600 s-1. Platelet-collagen interactions were estimated by counting the radioactivity in deposited platelets and by quantitative morphometry. When the perfusate consisted of normal platelets suspended in normal plasma, platelet deposition on the collagen was 24.7 +/- 3.6 X 10(6)/cm2 (mean +/- SEM, n = 6). Significantly less deposition (16 +/- 2.3) was observed when vWD platelets were substituted for normal platelets. In mixtures containing vWD plasma, significantly greater deposition (9 +/- 2.2) was obtained with normal than with vWD platelets (1 +/- 0.4) demonstrating a role for platelet vWF in mediating the deposition of platelets on collagen. Morphometric analysis confirmed these data. Our findings indicate that platelet, as well as plasma, vWF mediates platelet-collagen interactions at a high shear rate.

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