Effects of Starch Volume Expanders on Blood Viscosity and Vascular Endothelial Markers

2010 ◽  
Author(s):  
Andrew M. Walker ◽  
Kogan Lee ◽  
Kristina D. Rinker ◽  
Robert D. Shepherd ◽  
Gary M. Dobson ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Viscosity ◽  
Leukocyte Adhesion ◽  
Shear Thickening ◽  
Vascular Endothelial ◽  
Flow Loop ◽  
Aortic Endothelial Cells ◽  
Appreciable Increase ◽  
Human Aortic Endothelial Cells ◽  
Dose Dependent

The intravenous fluid of choice for acute blood volume replacement remains controversial. We focus here on the two hydroxyethyl (HES) available in Canada: HES 130/0.40 (Voluven®) and HES 260/0.45 (Pentaspan®). Although information regarding their pharmacokinetic and risk/benefit profiles are available, how the infusion of these fluids could affect blood viscosity and vascular endothelial function in humans is largely unknown. Dynamic viscosity was measured at 21°C and 37°C through capillary viscometry. The HES solutions were driven through a closed flow loop at room temperature (21°C). Viscosity at 21°C was 7.62 centipoise (cP) for HES 260/0.45 and 2.73 cP for HES 130/0.40 decreasing to 4.23 cP for HES 260/0.45 and 1.72 cP for HES 130/0.40 at 37°C. Analysis of viscous behaviour through pipe flow found that HES 260/0.45 displayed marginal variations in viscosity suggesting Newtonian behaviour across our range of Re measured. HES 130/0.40 displayed an appreciable increase in viscosity at higher Re suggesting the presence of shear thickening behaviour. Human aortic endothelial cells (HAEC) and human microvascular endothelial cells (HMVEC) were exposed to the HES solutions and saline to identify chemical effects on vascular endothelium. Western blot quantification showed that E-selectin was the leukocyte adhesion receptor that was most strongly affected, and this was not dose dependent. Interestingly, HAEC and HMVEC had different responses to HES treatment, suggesting that different vascular tissues may have different outcomes to HES infusion. Protein expression in HMVEC decreased when exposed to both HES solutions.

scholarly journals Conjugated Metabolites of Hydroxytyrosol and Tyrosol Contribute to the Maintenance of Nitric Oxide Balance in Human Aortic Endothelial Cells at Physiologically Relevant Concentrations

Molecules ◽  
2021 ◽  
Vol 26 (24) ◽  
pp. 7480
Author(s):  
Gabriele Serreli ◽  
Melanie Le Sayec ◽  
Camilla Diotallevi ◽  
Alice Teissier ◽  
Monica Deiana ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Leukocyte Adhesion ◽  
Virgin Olive Oil ◽  
Guanosine Monophosphate ◽  
No Production ◽  
Aortic Endothelial Cells ◽  
Human Aortic Endothelial Cells ◽  
Conjugated Metabolites ◽  
Aortic Endothelial

Nitric oxide (NO) is an important signaling molecule involved in many pathophysiological processes. NO mediates vasodilation and blood flow in the arteries, and its action contributes to maintaining vascular homeostasis by inhibiting vascular smooth muscle contraction and growth, platelet aggregation, and leukocyte adhesion to the endothelium. Dietary antioxidants and their metabolites have been found to be directly and/or indirectly involved in the modulation of the intracellular signals that lead to the production of NO. The purpose of this study was to investigate the contribution of conjugated metabolites of hydroxytyrosol (HT) and tyrosol (TYR) to the release of NO at the vascular level, and the related mechanism of action, in comparison to their parental forms. Experiments were performed in human aortic endothelial cells (HAEC) to evaluate the superoxide production, the release of NO and production of cyclic guanosine monophosphate (cGMP), the activation of serine/threonine-protein kinase 1 (Akt1), and the activation state of endothelial nitric oxide synthase (eNOS). It was observed that the tested phenolic compounds enhanced NO and cGMP concentration, inhibiting its depletion caused by superoxide overproduction. Moreover, some of them enhanced the activation of Akt (TYR, HT metabolites) and eNOS (HT, HVA, TYR-S, HT-3S). Overall, the obtained data showed that these compounds promote NO production and availability, suggesting that HT and TYR conjugated metabolites may contribute to the effects of parental extra virgin olive oil (EVOO) phenolics in the prevention of cardiovascular diseases.

scholarly journals Membrane-bound Progesterone Receptor Expression in Human Aortic Endothelial Cells

2003 ◽  
Vol 51 (8) ◽  
pp. 1049-1055 ◽  
Author(s):  
Brenda H. Welter ◽  
Elizabeth L. Hansen ◽  
Karla J. Saner ◽  
Yangzhan Wei ◽  
Thomas M. Price
Keyword(s):  
Cell Cycle ◽  
Endothelial Cells ◽  
Plasma Membrane ◽  
Progesterone Receptor ◽  
Progesterone Receptors ◽  
Vascular Endothelial ◽  
Aortic Endothelial Cells ◽  
Membrane Bound ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

Observational studies demonstrate that estradiol and progesterone affect vasoreactivity. In animal studies, progesterone treatment causes immediate relaxation of precontracted arteries with inhibition of calcium influx in vascular endothelial and smooth muscle cells, suggesting a non-genomic mechanism of action. In this study we investigated the presence of novel membrane-bound progesterone receptors in human aortic endothelial cells and correlated the expression with cell-cycle stage. Western blotting analysis with an antibody directed to the hormone-binding domain of the classic progesterone receptors shows predominant bands at 100 and 60 kD, whereas analysis with an antibody to the DNA-binding region shows only the 100-kD band. In contrast, classic nuclear progesterone receptors B and A are identified at 116 and 94 kD in similarly processed T47D cells. Both novel bands localize to the membrane fraction after differential centrifugation. Plasma membrane-bound progesterone receptor was further shown with immunofluorescent antibody and ligand-binding studies in a small percentage of human aortic endothelial cells. Fluorescent activated cell sorting demonstrated that approximately 8% of the human aortic endothelial cells expressed a plasma membrane progesterone receptor and that a greater percentage of the expressing cells were in the G2/M-phase of the cell cycle. Treatment with progesterone conjugated to BSA did not show any significant cell-cycle changes. Plasma membrane-bound progesterone receptor in vascular endothelial cells may regulate the non-genomic actions of progesterone, and expression of the receptor appears to vary with cell cycle stage.

Lipolysis products from triglyceride-rich lipoproteins increase endothelial permeability, perturb zonula occludens-1 and F-actin, and induce apoptosis

2007 ◽  
Vol 292 (6) ◽  
pp. H2745-H2753 ◽  
Author(s):  
Larissa Eiselein ◽  
Dennis W. Wilson ◽  
Michael W. Lamé ◽  
John C. Rutledge
Keyword(s):  
Endothelial Cells ◽  
Lipoprotein Lipase ◽  
Endothelial Permeability ◽  
Vascular Endothelial ◽  
Aortic Endothelial Cells ◽  
Zonula Occludens ◽  
Vascular Endothelial Cadherin ◽  
Zonula Occludens 1 ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

Products generated from lipoprotein lipase-mediated hydrolysis of triglyceride-rich lipoproteins (TGRL) are reported to increase endothelial layer permeability. We hypothesize that these increases in permeability result from the active rearrangement and dissolution of the junctional barrier in human aortic endothelial cells, as well as induction of the apoptotic cascade. Human aortic endothelial cells were treated with TGRL lipolysis products generated from coincubation of human TGRL plus lipoprotein lipase. Measurement of transendothelial electrical resistance demonstrated a time-dependent decrease in endothelial barrier function in response to TGRL lipolysis products. Immunofluorescent localization of zonula occludens-1 (ZO-1) showed radial rearrangement along cell borders after 1.5 h of treatment with lipolysis products. A concurrent redistribution of F-actin from the cell body to the cell margins was observed via rhodamine phalloidin staining. Immunofluorescent imaging for occludin and vascular endothelial cadherin showed that these proteins relocalize as well, although these changes are less prominent than for ZO-1. Western analysis of cells exposed to lipolysis products for 3 h revealed the fragmentation of ZO-1, a reduction in occludin, and no change of vascular endothelial cadherin. Lipolysis products also increased caspase-3 activity and induced nuclear fragmentation. Treatments did not cause oncosis in cells at any point during the incubation. These results demonstrate that TGRL lipolysis products play an important role in the regulation of endothelial permeability, the organization of the actin cytoskeleton, the localization and expression of junctional proteins, especially ZO-1, and the induction of apoptosis.

scholarly journals Orai–vascular endothelial-cadherin signaling complex regulates high-glucose exposure-induced increased permeability of mouse aortic endothelial cells

2021 ◽  
Vol 9 (1) ◽  
pp. e002085
Author(s):  
Yuan Wei ◽  
Suwen Bai ◽  
YanHeng Yao ◽  
Wenxuan Hou ◽  
Junwei Zhu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Membrane ◽  
High Glucose ◽  
Expression Level ◽  
Vascular Endothelial ◽  
Aortic Endothelial Cells ◽  
Downstream Signaling ◽  
Signaling Complex ◽  
Aortic Endothelium ◽  
Aortic Endothelial

IntroductionDiabetes-associated endothelial barrier function impairment might be linked to disturbances in Ca2+ homeostasis. To study the role and molecular mechanism of Orais–vascular endothelial (VE)-cadherin signaling complex and its downstream signaling pathway in diabetic endothelial injury using mouse aortic endothelial cells (MAECs).Research design and methodsThe activity of store-operated Ca2+ entry (SOCE) was detected by calcium imaging after 7 days of high-glucose (HG) or normal-glucose (NG) exposure, the expression levels of Orais after HG treatment was detected by western blot analysis. The effect of HG exposure on the expression of phosphorylated (p)-VE-cadherin and VE-cadherin on cell membrane was observed by immunofluorescence assay. HG-induced transendothelial electrical resistance was examined in vitro after MAECs were cultured in HG medium. FD-20 permeability was tested in monolayer aortic endothelial cells through transwell permeability assay. The interactions between Orais and VE-cadherin were detected by co-immunoprecipitation and immunofluorescence technologies. Immunohistochemical experiment was used to detect the expression changes of Orais, VE-cadherin and p-VE-cadherin in aortic endothelium of mice with diabetes.Results(1) The expression levels of Orais and activity of SOCE were significantly increased in MAECs cultured in HG for 7 days. (2) In MAECs cultured in HG for 7 days, the ratio of p-VE-cadherin to VE-cadherin expressed on the cell membrane and the FD-20 permeability in monolayer endothelial cells increased, indicating that intercellular permeability increased. (3) Orais and VE-cadherin can interact and enhance the interaction ratio through HG stimulation. (4) In MAECs cultured with HG, the SOCE activator ATP enhanced the expression level of p-VE-cadherin, and the SOCE inhibitor BTP2 decreased the expression level of p-VE-cadherin. (5) Significantly increased expression of p-VE-cadherin and Orais in the aortic endothelium of mice with diabetes.ConclusionHG exposure stimulated increased expression of Orais in endothelial cells, and increased VE-cadherin phosphorylation through Orais–VE-cadherin complex and a series of downstream signaling pathways, resulting in disruption of endothelial cell junctions and initiation of atherosclerosis.

Modulation of calcium homeostasis in cultured rat aortic endothelial cells by intracellular acidification

1993 ◽  
Vol 265 (4) ◽  
pp. H1424-H1433 ◽  
Author(s):  
R. C. Ziegelstein ◽  
L. Cheng ◽  
P. S. Blank ◽  
H. A. Spurgeon ◽  
E. G. Lakatta ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Cytosolic Calcium ◽  
Ph Sensitive ◽  
Vascular Endothelial ◽  
Intracellular Acidification ◽  
Cytosolic Ph ◽  
Aortic Endothelial Cells ◽  
Endothelial Monolayers ◽  
Aortic Endothelial

Acidosis produces vasodilation in a process that may involve the vascular endothelium. Because synthesis and release of endothelium-derived vasodilatory substances are linked to an increase in cytosolic calcium concentration ([Ca2+]i), we examined the effect of intracellular acidification on cultured rat aortic endothelial cells loaded either with the pH-sensitive probe carboxy-seminaphthorhodafluor-1 or the Ca(2+)-sensitive fluorescent probe indo 1. The basal cytosolic pH (pHi) of endothelial monolayers in a 5% CO2-HCO3- buffer was 7.27 +/- 0.02 and that in a bicarbonate-free solution was 7.22 +/- 0.03. Acidification was induced either by removal of NH4Cl (delta pHi = -0.10 +/- 0.02), changing from a bicarbonate-free to a 5% CO2-HCO3(-)-buffered solution at constant buffer pH (delta pHi = -0.18 +/- 0.03), or changing from a 5% to a 20% CO2-HCO3- solution (delta pHi = -0.27 +/- 0.07). Regardless of the method used, intracellular acidification increased [Ca2+]i as indexed by indo 1 fluorescence. The increase in [Ca2+]i induced by changing from a 5 to a 20% CO2-HCO3- solution was not significantly altered by removal of buffer Ca2+ either before or after depletion of bradykinin- and thapsigargin-sensitive intracellular Ca2+ stores. Thus intracellular acidification of vascular endothelial cells releases Ca2+ into the cytosol either from pH-sensitive intracellular buffer sites, mitochondria, or from bradykinin- and thapsigargin-insensitive intracellular stores. This Ca2+ mobilization may be linked to endothelial synthesis and release of vasodilatory substances during acidosis.

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