Regulation of capillary hydraulic conductivity in response to an acute change in shear

2005 ◽  
Vol 289 (5) ◽  
pp. H2126-H2135 ◽  
Author(s):  
Min-ho Kim ◽  
Norman R. Harris ◽  
John M. Tarbell
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Hydraulic Conductivity ◽  
Flow Shear ◽  
Fluid Filtration ◽  
Acute Change ◽  
Acute Changes ◽  
Mesenteric Microvessels

The effects of mechanical perturbations (shear stress, pressure) on microvascular permeability primarily have been examined in micropipette-cannulated vessels or in endothelial monolayers in vitro. The objective of this study is to determine whether acute changes in blood flow shear stress might influence measurements of hydraulic conductivity ( Lp) in autoperfused microvessels in vivo. Rat mesenteric microvessels were observed via intravital microscopy. Occlusion of a third-order arteriole with a micropipette was used to divert and increase flow through a nonoccluded capillary or fourth-order arteriolar branch. Transvascular fluid filtration rate in the branching vessel was measured with a Landis technique. Flow (shear)-induced increases in Lp disappeared within 20–30 s of the removal of the shear and could be eliminated with nitric oxide synthase inhibition. The shear-induced increase in Lp was greater in capillaries compared with terminal arterioles. An acute change in shear may regulate Lp by a nitric oxide-dependent mechanism that displays heterogeneity within a microvascular network.

scholarly journals Endothelial pulsatile shear stress is a backstop for COVID-19

2020 ◽  
Vol 4 (4) ◽  
pp. 391-399
Author(s):  
Marvin A. Sackner ◽  
Jose A. Adams
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Physical Inactivity ◽  
Muscular Activity ◽  
The Body ◽  
Diverse Populations ◽  
Extensive Investigation ◽  
Pulsatile Shear Stress

There has not been any means to inhibit replication of the SARS-CoV-2 virus responsible for the rapid, deadly spread of the COVID-19 pandemic and an effective, safe, tested across diverse populations vaccine still requires extensive investigation. This review deals with the repurpose of a wellness technology initially fabricated for combating physical inactivity by increasing muscular activity. Its action increases pulsatile shear stress (PSS) to the endothelium such that the bioavailability of nitric oxide (NO) and other mediators are increased throughout the body. In vitro evidence indicates that NO inhibits SARS-CoV-2 virus replication but there are no publications of NO delivery to the virus in vivo. It will be shown that increased PSS has potential in vivo to exert anti-viral properties of NO as well as to benefit endothelial manifestations of COVID-19 thereby serving as a safe and effective backstop.

Evidence of nitric oxide, a flow-dependent factor, being a trigger of liver regeneration in rats

1998 ◽  
Vol 76 (12) ◽  
pp. 1072-1079 ◽  
Author(s):  
H Helen Wang ◽  
W Wayne Lautt
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Liver Regeneration ◽  
Partial Hepatectomy ◽  
Cultured Cells ◽  
Portal Blood Flow ◽  
Liver Weight ◽  
Proliferative Effect

The hypothesis tested was that the hemodynamic consequence of partial hepatectomy (PHX) triggers the cascade of events that leads to liver regeneration. After PHX, all the portal flow must go through the remaining vascular bed, thus producing increased shear stress and release of nitric oxide (NO), which then initiates the next stages of the regeneration process. As an index of triggering of the regeneration cascade, we used an in vitro bioassay detecting the appearance of proliferating factors (PFs; various growth factors, cytokines, and hormones) in plasma 4 h after two-thirds PHX in rats. PF levels, assessed using proliferation of cultured hepatocytes, were elevated in two-thirds PHX rats, fully blocked by the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME), and restored by L-arginine. L-NAME inhibited liver weight restoration at 48 h but resulted in high mortality. L-NAME lacked toxic effects in non-PHX rats. NO was directly antiproliferative on cultured cells, suggesting that the proliferative effect of NO in vivo was secondary to the activation of other proliferative stimuli. The data support the hypothesis that vascular shear stress induced release of NO following PHX serves as a primary trigger to initiate the regeneration process.Key words: shear stress, portal blood flow, hyperplasia, hepatic partial hepatectomy.

THE INFLUENCE OF STRESS CONDITIONS ON THE UPTAKE OF 131I BY THE RAT THYROID

1954 ◽  
Vol 11 (4) ◽  
pp. 305-313 ◽  
Author(s):  
F. E. BADRICK ◽  
R. W. BRIMBLECOMBE ◽  
JEAN M. REISS ◽  
M. REISS
Keyword(s):  
Anterior Pituitary ◽  
Acute Stress ◽  
Inhibitory Effect ◽  
Stress Conditions ◽  
Thyrotrophic Hormone ◽  
Acute Change ◽  
Acute Changes ◽  
Rat Thyroid

SUMMARY The uptake of 131I by the thyroid of the rat has been investigated under various conditions of stress. The acute change always consists in a considerable reduction of the rate of uptake of 131I irrespective of the nature of the stress. This acute inhibition in the uptake of 131I is independent of the anterior pituitary lobe, since it occurs in the normal and hypophysectomized animal alike. It is also independent of the presence of the adrenals. The inhibition of the uptake of 131I by the thyroids occurs in vivo only; their ability to take up 131I in vitro is not impaired. All the acute changes seen under stress conditions can be readily reproduced by treatment with adrenaline, which shows the same inhibitory effect on normal and hypophysectomized animals, the action being equally transitory. It is suggested that the acute changes in thyroid function seen under stress conditions are entirely independent of the anterior pituitary and are caused by increased release of vasoconstrictor substances. An increased uptake rate of 131I by the thyroid was seen 24 hr after the acute stress. This was thought to be caused by a compensatory increase in the secretion of thyrotrophic hormone by the anterior pituitary.

scholarly journals The endothelial glycocalyx mediates shear-induced changes in hydraulic conductivity

2009 ◽  
Vol 296 (5) ◽  
pp. H1451-H1456 ◽  
Author(s):  
Sandra V. Lopez-Quintero ◽  
Ronny Amaya ◽  
Manolis Pahakis ◽  
John M. Tarbell
Keyword(s):  
Shear Stress ◽  
Hydraulic Conductivity ◽  
Fluid Shear Stress ◽  
Endothelial Glycocalyx ◽  
In Vivo Studies ◽  
Induced Response ◽  
No Production ◽  
Block Shear

Recent in vitro and in vivo studies have reported fluid shear stress-induced increases in endothelial layer hydraulic conductivity ( Lp) that are mediated by an increased production of nitric oxide (NO). Other recent studies have shown that NO induction by shear stress is mediated by the glycocalyx that decorates the surface of endothelial cells. Here we find that a selective depletion of the major components of the glycocalyx with enzymes can block the shear stress-induced response of Lp. Heparinase and hyaluronidase block shear-induced increases in Lp, which is consistent with their effects on NO production. But chondroitinase, which does not suppress shear-induced NO production, also inhibits shear-induced Lp. A further surprise is that treatment with the general proteolytic enzyme pronase does not suppress the shear Lp response. We also find that heparinase does not alter baseline Lp significantly, whereas chondroitinase, hyaluronidase, and pronase increase it significantly.

Transendothelial flow inhibits neutrophil transmigration through a nitric oxide-dependent mechanism: potential role for cleft shear stress

2007 ◽  
Vol 293 (5) ◽  
pp. H2904-H2910 ◽  
Author(s):  
Alan R. Burns ◽  
Zhilan Zheng ◽  
Said H. Soubra ◽  
Jie Chen ◽  
Rolando E. Rumbaut
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Umbilical Vein ◽  
Human Neutrophils ◽  
No Production ◽  
No Donor ◽  
Fluid Filtration ◽  
Luminal Flow ◽  
Dependent Mechanism

Endothelial cells in vivo are well known to respond to parallel shear stress induced by luminal blood flow. In addition, fluid filtration across endothelium (transendothelial flow) may trigger nitric oxide (NO) production, presumably via shear stress within intercellular clefts. Since NO regulates neutrophil-endothelial interactions, we determined whether transendothelial flow regulates neutrophil transmigration. Interleukin-1β-treated human umbilical vein endothelial cell (HUVEC) monolayers cultured on a polycarbonate filter were placed in a custom chamber with or without a modest hydrostatic pressure gradient (ΔP, 10 cmH2O) to induce transendothelial flow. In other experiments, cells were studied in a parallel plate flow chamber at various transendothelial flows (ΔP = 0, 5, and 10 cmH2O) and luminal flows (shear stress of 0, 1, and 2 dyn/cm2). In the absence of luminal flow, transendothelial flow reduced transmigration of freshly isolated human neutrophils from 57% to 14% ( P < 0.05) and induced an increase in NO detected with a fluorescent assay (DAF-2DA). The NO synthase inhibitor l-NAME prevented the effects of transendothelial flow on neutrophil transmigration, while a NO donor (DETA/NO, 1 mM) inhibited neutrophil transmigration. Finally, in the presence of luminal flow (1 and 2 dyn/cm2), transendothelial flow also inhibited transmigration. On the basis of HUVEC morphometry and measured transendothelial volume flow, we estimated cleft shear stress to range from 49 to 198 dyn/cm2. These shear stress estimates, while substantial, are of similar magnitude to those reported by others with similar analyses. These data are consistent with the hypothesis that endothelial cleft shear stress inhibits neutrophil transmigration via a NO-dependent mechanism.

scholarly journals In Vitro and In Vivo Anti-Inflammatory Effects of Sulfated Polysaccharides Isolated from the Edible Brown Seaweed, Sargassum fulvellum

Marine Drugs ◽  
2021 ◽  
Vol 19 (5) ◽  
pp. 277
Author(s):  
Lei Wang ◽  
Hye-Won Yang ◽  
Ginnae Ahn ◽  
Xiaoting Fu ◽  
Jiachao Xu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Brown Seaweed ◽  
Sulfated Polysaccharides ◽  
Raw 264.7 ◽  
Raw 264.7 Macrophages ◽  
Sargassum Fulvellum ◽  
Pharmaceutical Industries ◽  
Anti Inflammatory

In the present study, the in vitro and in vivo anti-inflammatory effects of the sulfated polysaccharides isolated from Sargassum fulvellum (SFPS) were evaluated in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages and zebrafish. The results indicated that SFPS improved the viability of LPS-stimulated RAW 264.7 macrophages from 80.02 to 86.80, 90.09, and 94.62% at the concentration of 25, 50, and 100 µg/mL, respectively. Also, SFPS remarkably and concentration-dependently decreased the production levels of inflammatory molecules including nitric oxide (NO), tumor necrosis factor-alpha, prostaglandin E2, interleukin-1 beta, and interleukin-6 in LPS-treated RAW 264.7 macrophages. In addition, SFPS significantly inhibited the expression levels of cyclooxygenase-2 and inducible nitric oxide synthase in LPS-treated RAW 264.7 macrophages. Furthermore, the in vivo test results indicated that SFPS improved the survival rate of LPS-treated zebrafish from 53.33 to 56.67, 60.00, and 70.00% at the concentration of 25, 50, and 100 µg/mL, respectively. In addition, SFPS effectively reduced cell death, reactive oxygen species, and NO levels in LPS-stimulated zebrafish. Taken together, these results suggested that SFPS possesses strong in vitro and in vivo anti-inflammatory activities, and could be used as an ingredient to develop anti-inflammatory agents in the functional food and pharmaceutical industries.

scholarly journals Rapid Fabrication of Microfluidic Devices for Biological Mimicking: A Survey of Materials and Biocompatibility

Micromachines ◽  
2021 ◽  
Vol 12 (3) ◽  
pp. 346
Author(s):  
Hui Ling Ma ◽  
Ana Carolina Urbaczek ◽  
Fayene Zeferino Ribeiro de Souza ◽  
Paulo Augusto Gomes Garrido Carneiro Leão ◽  
Janice Rodrigues Perussi ◽  
...  
Keyword(s):  
Shear Stress ◽  
Cell Viability ◽  
Cellular Response ◽  
Fluid Shear Stress ◽  
Umbilical Vein ◽  
Microfluidic Devices ◽  
In Vitro Assays ◽  
Stress Effect

Microfluidics is an essential technique used in the development of in vitro models for mimicking complex biological systems. The microchip with microfluidic flows offers the precise control of the microenvironment where the cells can grow and structure inside channels to resemble in vivo conditions allowing a proper cellular response investigation. Hence, this study aimed to develop low-cost, simple microchips to simulate the shear stress effect on the human umbilical vein endothelial cells (HUVEC). Differentially from other biological microfluidic devices described in the literature, we used readily available tools like heat-lamination, toner printer, laser cutter and biocompatible double-sided adhesive tapes to bind different layers of materials together, forming a designed composite with a microchannel. In addition, we screened alternative substrates, including polyester-toner, polyester-vinyl, glass, Permanox® and polystyrene to compose the microchips for optimizing cell adhesion, then enabling these microdevices when coupled to a syringe pump, the cells can withstand the fluid shear stress range from 1 to 4 dyne cm2. The cell viability was monitored by acridine orange/ethidium bromide (AO/EB) staining to detect live and dead cells. As a result, our fabrication processes were cost-effective and straightforward. The materials investigated in the assembling of the microchips exhibited good cell viability and biocompatibility, providing a dynamic microenvironment for cell proliferation. Therefore, we suggest that these microchips could be available everywhere, allowing in vitro assays for daily laboratory experiments and further developing the organ-on-a-chip concept.

scholarly journals Phaseolin Attenuates Lipopolysaccharide-Induced Inflammation in RAW 264.7 Cells and Zebrafish

Biomedicines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 420
Author(s):  
Su-Jung Hwang ◽  
Ye-Seul Song ◽  
Hyo-Jong Lee
Keyword(s):  
Nitric Oxide ◽  
Nuclear Translocation ◽  
Raw 264.7 Cells ◽  
Network Pharmacology ◽  
Raw 264.7 ◽  
Dependent Manner ◽  
Bioactive Constituents

Kushen (Radix Sophorae flavescentis) is used to treat ulcerative colitis, tumors, and pruritus. Recently, phaseolin, formononetin, matrine, luteolin, and quercetin, through a network pharmacology approach, were tentatively identified as five bioactive constituents responsible for the anti-inflammatory effects of S. flavescentis. However, the role of phaseolin (one of the primary components of S. flavescentis) in the direct regulation of inflammation and inflammatory processes is not well known. In this study, the beneficial role of phaseolin against inflammation was explored in lipopolysaccharide (LPS)-induced inflammation models of RAW 264.7 macrophages and zebrafish larvae. Phaseolin inhibited LPS-mediated production of nitric oxide (NO) and the expression of inducible nitric oxide synthase (iNOS), without affecting cell viability. In addition, phaseolin suppressed pro-inflammatory mediators such as cyclooxygenase 2 (COX-2), interleukin-1β (IL-1β), tumor necrosis factor α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), and interleukin-6 (IL-6) in a dose-dependent manner. Furthermore, phaseolin reduced matrix metalloproteinase (MMP) activity as well as macrophage adhesion in vitro and the recruitment of leukocytes in vivo by downregulating Ninjurin 1 (Ninj1), an adhesion molecule. Finally, phaseolin inhibited the nuclear translocation of nuclear factor-kappa B (NF-κB). In view of the above, our results suggest that phaseolin could be a potential therapeutic candidate for the management of inflammation.

scholarly journals Novel Insights on the Role of Nitric Oxide in the Ovary: A Review of the Literature

2021 ◽  
Vol 18 (3) ◽  
pp. 980
Author(s):  
Maria Cristina Budani ◽  
Gian Mario Tiboni
Keyword(s):  
Nitric Oxide ◽  
In Vivo Studies ◽  
Published Data ◽  
Vitro Fertilization ◽  
Peripheral Neurons ◽  
Relevant Role ◽  
Oocyte Meiotic Maturation

Nitric oxide (NO) is formed during the oxidation of L-arginine to L-citrulline by the action of multiple isoenzymes of NO synthase (NOS): neuronal NOS (nNOS), endotelial NOS (eNOS), and inducible NOS (iNOS). NO plays a relevant role in the vascular endothelium, in central and peripheral neurons, and in immunity and inflammatory systems. In addition, several authors showed a consistent contribution of NO to different aspects of the reproductive physiology. The aim of the present review is to analyse the published data on the role of NO within the ovary. It has been demonstrated that the multiple isoenzymes of NOS are expressed and localized in the ovary of different species. More to the point, a consistent role was ascribed to NO in the processes of steroidogenesis, folliculogenesis, and oocyte meiotic maturation in in vitro and in vivo studies using animal models. Unfortunately, there are few nitric oxide data for humans; there are preliminary data on the implication of nitric oxide for oocyte/embryo quality and in-vitro fertilization/embryo transfer (IVF/ET) parameters. NO plays a remarkable role in the ovary, but more investigation is needed, in particular in the context of human ovarian physiology.

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