TY - JOUR. T1 - Magnitude-dependent regulation of pulmonary endothelial cell barrier function by cyclic stretch. AU - Birukov, Konstantin G.. AU - Jacobson, Jeffrey R.. AU - Flores, Alejandro A.. AU - Ye, Shui Q.. AU - Birukova, Anna A.. AU - Verin, Alexander D.. AU - Garcia, Joe G.N.. PY - 2003/10/1. Y1 - 2003/10/1. N2 - Ventilator-induced lung injury syndromes are characterized by profound increases in vascular leakiness and activation of inflammatory processes. To explore whether excessive cyclic stretch (CS) directly causes vascular barrier disruption or enhances endothelial cell sensitivity to edemagenic agents, human pulmonary artery endothelial cells (HPAEC) were exposed to physiologically (5% elongation) or pathologically (18% elongation) relevant levels of strain. CS produced rapid (10 min) increases in myosin light chain (MLC) phosphorylation, activation of p38 and extracellular signal-related kinase 1/2 MAP kinases, and actomyosin remodeling. Acute (15 min) and chronic (48 h) CS ...
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TY - JOUR. T1 - Fibrinogen-γ C-Terminal fragments induce endothelial barrier dysfunction and microvascular leak via integrin-mediated and RhoA-dependent mechanism. AU - Guo, Mingzhang. AU - Daines, Dayle. AU - Tang, Jing. AU - Shen, Qiang. AU - Perrin, Rachel M.. AU - Takada, Yoshikazu. AU - Yuan, Sarah Y.. AU - Wu, Mack H.. PY - 2009/3. Y1 - 2009/3. N2 - Objectives - The purposes of this study were to characterize the direct effect of the C-terminal fragment of fibrinogen γ chain (γC) on microvascular endothelial permeability and to examine its molecular mechanism of action. Methods and Results-Intravital microscopy was performed to measure albumin extravasation in intact mesenteric microvasculature, followed by quantification of hydraulic conductivity in single perfused micro vessels. Transendothelial electric resistance was measured in microvascular endothelial cells in combination with immunoblotting and immunocytochemistry. The results show that γC induced time- and ...
Inhibitory effects of sasanquasaponin on over-expression of ICAM-1 and on enhancement of capillary permeability induced by burns in rats. - Qiren Huang, Lijian Shao, Ming He, Heping Chen, Dan Liu, Yongming Luo, Yucheng Dai
Vascular permeability factor (VPF) is a 40-kilodalton disulfide-linked dimeric glycoprotein that is active in increasing blood vessel permeability, endothelial cell growth, and angiogenesis. These properties suggest that the expression of VPF by tumor cells could contribute to the increased neovascularization and vessel permeability that are associated with tumor vasculature. The cDNA sequence of VPF from human U937 cells was shown to code for a 189-amino acid polypeptide that is similar in structure to the B chain of platelet-derived growth factor (PDGF-B) and other PDGF-B-related proteins. The overall identity with PDGF-B is 18%. However, all eight of the cysteines in PDGF-B were found to be conserved in human VPF, an indication that the folding of the two proteins is probably similar. Clusters of basic amino acids in the COOH-terminal halves of human VPF and PDGF-B are also prevalent. Thus, VPF appears to be related to the PDGF/v-sis family of proteins.
Our finding that short-term treatment with imatinib protects against endothelial barrier dysfunction and edema formation provides first mechanistic insight regarding previous case reports on patients in whom initiation of imatinib treatment was followed by fast resolution of pulmonary edema.5,11 Combining in vitro and in vivo measurements of endothelial barrier dysfunction and vascular leakage, we found that imatinib protects against edema formation by enforcing the endothelial barrier. Although edema formation and vascular leakage may also be affected by changes in blood pressure, microvascular perfusion, or vascular remodeling, these factors are less likely to underlie the protective effect of imatinib. Alteration of blood pressure and microvascular perfusion as explanation for edema resolution was excluded in this study, because (1) imatinib did not affect systemic blood pressure in an experimental set-up similar to the Miles assay or Kfc measurements, (2) the pressure and the flow in the ...
Background and Objective: Impairment of the regulation of tissue fluid homeostasis and migration of blood cells across the endothelial barrier are crucial factors in the pathogenesis of acute lung injury (ALI). Thus, a goal for treatment of ALI is to target the pathways that lead to profound dysregulation of the restrictive endothelial barrier, and thereby restore lung microvascular endothelial barrier function and inhibit protein-rich tissue fluid accumulation. Here we test the hypothesis that epigenetic modifiers TSA (Trichostatin-A, a HDAC inhibitor) and Aza (5-aza-2-deoxycytidine, a DNA methyl transferase inhibitor) together inhibit the LPS/thrombin induced eNOS/RhoA signaling and restore AJ integrity and diminished endothelial hyperpermeability.. Methods and Results: The signaling, AJ integrity and endothelial permeability were assessed by RT-PCR and western blot analysis; transendothelial resistance (TER) and lung endothelial permeability were measured by capillary filtration coefficient ...
The control of fluid introduction into and out of body conduits such as vessels, is of great concern in medicine. As the development of more particular treatments to vessels and organs continues it is apparent that controlled introduction and removal of fluids is necessary. Fluid delivery and removal from such sites, usually referred to as irrigation and aspiration, using fluid exchange devices that control also need to be considerate of potential volume and/or pressure in the vessel or organ are described together with catheter and lumen configurations to achieve the fluid exchange. The devices include several electrically or mechanically controlled embodiments and produce both controlled and localized flow with defined volume exchange ratios for fluid management. The applications in medicine include diagnostic, therapeutic, imaging, and uses for the introduction or removal of concentrations of emboli within body cavities.
Dr. Garcia is an authority on the genetic basis of inflammatory lung disease (with an emphasis on health disparities) and on the mechanistic basis of lung vascular permeability. Using bench-to-bedside approaches, his lab has explored novel methods to prevent vascular leak and to restore endothelial cell barrier function and vascular integrity. This expertise in lung inflammation and vascular permeability provides a natural linkage to interrogation of lung vascular contribution to the development of lung metastases.. Leveraging their genomic expertise, in recent years, Dr. Garcias lab has identified vascular genes whose products are key participants in inflammatory lung injury that also play a role in cancer development. They have developed lung endothelial inflammatory gene expression profiles as well as diagnostic gene signatures influenced by MYLK and NAMPT that impact lung and breast cancer prognosis. This work with NAMPT led to development of a therapeutic NAMPT neutralizing antibody that ...
AJs disassemble and reassemble in endothelial monolayers in response to proinflammatory mediators such as thrombin.29 AJ reassembly precedes the restoration of vascular endothelial barrier integrity.29-31 However, the signals responsible for recovery of endothelial barrier function are incompletely understood. Herein, we addressed the basis for the reformation of AJs and the subsequent recovery of endothelial barrier function. Reassembly of AJs in epithelial cells has been linked to activation of Rho GTPases.32 The Rho family of proteins, known to translocate to membranes on activation, is responsible for actin cytoskeleton rearrangements affecting chemotaxis, cell motility, vesicular trafficking, and cell-cell adhesion.22 We assessed the time course of activation of Rho GTPases after thrombin and found that Cdc42 was activated during the phase of AJ reformation. This finding is consistent with evidence that Cdc42 was not involved in signaling the increase in endothelial permeability induced by ...
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These studies are the first to show that the anti-angiogenic VEGF-A165b does not disturb the junctional occupancy of VE-cadherin or induce paracellular tracer leakage in the human placental microvascular bed and HUVEC monolayers. Indeed, VEGF-A165b (at a 2-fold concentration) can block/reverse VEGF-A165a-mediated increases in feto-placental endothelial permeability to macromolecules (75 kDa) and loss of VE-cadherin from AJs. In these experiments, PlGF did not affect endothelial integrity, VE-cadherin localization and permeability when added singly; however, it could prevent the rescue of VEGF-A165a-mediated effects by VEGF-A165b.. The similarities between the observed induced changes in both fetal endothelial cell cultures and the more physiological and complex perfused microvascular bed are re-assuring. Placental microvessels showed a robust response to a 30 min perfusion of exogenous VEGF-A165a, with loss of VE-cadherin and increased vascular leak of 76 kDa dextrans. These changes were not ...
A role for NRP1 in driving the effects of VEGF on vascular permeability was revealed in experiments in which NRP1 and VEGF receptor 2 (VEGFR2) were cotransfected (23), and was recently confirmed with the use of NRP1 inhibitors (24). The capacity of VEGF to promote tumor vessel leakiness (25) is actually the first property that led to the identification of this factor [initially described as the vascular permeability factor (26)]. A VEGF-like effect of CendR through its binding to NRP1 could therefore account for an increase in the tumor vessel surface of exchange and for a global elevation in vascular permeability, which is beneficial for the penetration of small drugs and macromolecules. The limitation of the number and capacity of receptors for targeted ligands is also less acute, because generic drug transport pathways are made available through paracellular permeability (passage between endothelial cells that involves localized disruption of cell junctions) or transcytosis (transport through ...
TY - JOUR. T1 - The ARP 2/3 complex mediates endothelial barrier function and recovery. AU - Belvitch, Patrick. AU - Brown, Mary E.. AU - Brinley, Brittany N.. AU - Letsiou, Eleftheria. AU - Rizzo, Alicia N.. AU - Garcia, Joe G.N.. AU - Dudek, Steven M.. PY - 2017/1/1. Y1 - 2017/1/1. N2 - Pulmonary endothelial cell (EC) barrier dysfunction and recovery is critical to the pathophysiology of acute respiratory distress syndrome. Cytoskeletal and subsequent cell membrane dynamics play a key mechanistic role in determination of EC barrier integrity. Here, we characterizAQe the actin related protein 2/3 (Arp 2/3) complex, a regulator of peripheral branched actin polymerization, in human pulmonary EC barrier function through studies of transendothelial electrical resistance (TER), intercellular gap formation, peripheral cytoskeletal structures and lamellipodia. Compared to control, Arp 2/3 inhibition with the small molecule inhibitor CK-666 results in a reduction of baseline barrier function (1,241±53 ...
Increased microvascular permeability to plasma proteins and neutrophil emigration are hallmarks of innate immunity and key features of numerous inflammatory disorders. Although neutrophils can promote microvascular leakage, the impact of vascular permeability on neutrophil trafficking is unknown. Here, through the application of confocal intravital microscopy, we report that vascular permeability-enhancing stimuli caused a significant frequency of neutrophil reverse transendothelial cell migration (rTEM). Furthermore, mice with a selective defect in microvascular permeability enhancement (VEC-Y685F-ki) showed reduced incidence of neutrophil rTEM. Mechanistically, elevated vascular leakage promoted movement of interstitial chemokines into the bloodstream, a response that supported abluminal-to-luminal neutrophil TEM. Through development of an in vivo cell labeling method we provide direct evidence for the systemic dissemination of rTEM neutrophils, and showed them to exhibit an activated ...
The research focus of Rolf Reeds group is on the how the extracellular matrix participates in determining the properties of the tumors and how this in turn is reflected in growth and metastasis. Additional foci have been on how collagen binding integrins influence these properties and also how tumor hypoxia does the same.
TY - JOUR. T1 - Nuclear targeting of beta-catenin and p120ctn during thrombin-induced endothelial barrier dysfunction. AU - Beckers, C.M.L.. AU - Garcia Vallejo, J.J.. AU - van Hinsbergh, V.W.M.. AU - van Nieuw Amerongen, G.P.. PY - 2008. Y1 - 2008. U2 - 10.1093/cvr/cvn127. DO - 10.1093/cvr/cvn127. M3 - Article. C2 - 18490349. VL - 79. SP - 679. EP - 688. JO - Cardiovascular Research. JF - Cardiovascular Research. SN - 0008-6363. IS - 4. ER - ...
The endothelial barrier function maintains vascular and tissue homeostasis, and therefore modulates many cardinal physiological processes such as angiogenesis, immune responses, and dynamic fluid exchanges throughout organs.
Purpose: Before metastasis, primary tumor can create a premetastatic niche in distant organ to facilitate the dissemination of tumor cells. In the premetastatic phase, the permeability of pulmonary vasculatures is increased to accelerate the extravasation of circulating tumor cells. However, it is not clear whether local miRNAs contribute to the vascular hyperpermeability of the premetastatic niche. Experimental Design: The expression of total miRNAs was determined using microarray in series of premetastatic lungs from tumor-bearing mice. Significantly differentially expressed miRNAs were identified and validated with qRT-PCR. Vascular permeability assays, vascular mimic systems, and orthotopic tumor models were used to investigate roles of selected miRNAs and target genes in premetastatic hyperpermeability. Results: We identified a miRNA signature in premetastatic lungs. Among these miRNAs, miR-30a, b, c, d and e were significantly attenuated. Subsequent investigations elucidated that lung ...
W.C. Sangren and C.W. Sheppard. A mathematical derivation of the exchange of a labelled substance between a liquid flowing in a vessel and an external compartment. Bull Math BioPhys, 15, 387-394, 1953. C.A. Goresky, W.H. Ziegler, and G.G. Bach. Capillary exchange modeling: Barrier-limited and flow-limited distribution. Circ Res 27: 739-764, 1970. J.B. Bassingthwaighte. A concurrent flow model for extraction during transcapillary passage. Circ Res 35:483-503, 1974. B. Guller, T. Yipintsoi, A.L. Orvis, and J.B. Bassingthwaighte. Myocardial sodium extraction at varied coronary flows in the dog: Estimation of capillary permeability by residue and outflow detection. Circ Res 37: 359-378, 1975. C.P. Rose, C.A. Goresky, and G.G. Bach. The capillary and sarcolemmal barriers in the heart--an exploration of labelled water permeability. Circ Res 41: 515, 1977. J.B. Bassingthwaighte, C.Y. Wang, and I.S. Chan. Blood-tissue exchange via transport and transformation by endothelial cells. Circ. Res. ...
This study provides compelling evidence that in marmoset EAE, which forms lesions strongly resembling those of MS, early changes in vascular permeability are associated with perivascular inflammatory cuffing and parenchymal microglial activation but precede the arrival of blood-derived monocytes tha …
The endothelium is the simple squamous epithelium that lines the innermost layer of the cardiovascular and lymphatic vessels and is continuous with the endocardial lining of the heart. Endothelial cells are active participants in a variety of vessel-related activities, including mechanical influences on blood flow, regulation of the transport of macromolecules and blood components from the interstitium to the lumen of the vessel, secretion of chemical mediators that influence the contractile state of the overlying smooth muscle, and contribution to capillary permeability. In addition, their smooth luminal surface facilitates efficient blood flow by reducing surface friction. The vascular endothelium is divided into arterial and venous endothelia, with additional differences between larger and smaller vessels.. The fenestrated endothelium, present in organs, such as the kidney and liver, that reabsorb water and small molecules or hormones, is characterized by the presence of circular windows in ...
Keywords: Thiazolidinediones, Rosiglitazone, Endothelial cells, Vascular permeability, Edema, Akt Background Cardiovascular disease is normally a leading trigger of loss of life related to atherosclerosis. Atherosclerosis takes place from a series of proinflammatory, proliferative, and procoagulatory procedures [1, 2]. Affected endothelial cell function has a vital function in the development of atherosclerosis [3]. Endothelial disorder can become characterized as an modification in cell migration and permeability. Endothelial cell migration entails the neovascularization of atherosclerotic plaques and causes plaques to become vulnerable. In addition, newly created small ships can provide an access for inflammatory cells [4]. Under physiological conditions, endothelial cells provide a buffer between blood ships and cells [5, 6]. However, inflammatory stimuli can increase endothelial permeability [6, 7] and enable the movement of macromolecules such as vascular endothelial growth element (VEGF), ...
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... utilizes cross flow as opposed to dead end feed flow, but feature smaller feed channels vs. tubular membranes.
Antigen combine with antibody. Mast cells & basophils release chemotactic agents. Histamine release causes vessel dilation and. Contraction of smooth muscles Result in increased capillary permeability and constriction of bronchioles ...
Optimal control of diabetes should achieve not only euglycemia and normal levels of glycosylated hemoglobin but also absence of the reversible concomitants of diabetes such as red cell rigidity, hyperlipidemia, increased capillary permeability, enlargement of the kidneys, proteinuria, etc. Unfortunately, in most patients consistent euglycemia cannot be assured even with two daily injections of insulin. However, self-measurement of blood glucose as a guide to insulin taken before each meal and at bedtime can, in selected patients, increase the frequency of normal glucose levels without undue hypoglycemia.. ...
My last post lead me to discover that resveratrol (RES) impacts the microbiome as shown in the diagram below. In particular, reduced unclassified bacteria. I had cover this in Resveratrol Revisited in 2015 suggested dosage 500-1000 mg/day strong antioxidant activity, antibacterial, antiviral, anticarcinogenic, anti-inflammatory, anti-allergic, and vasodilatory actions, inhibit lipid peroxidation, platelet aggregation, capillary permeability and fragility [2000]…
Blood Separators separate platelets from blood. A bearing is used to to provide rotary fluid exchange between the collection tray & the separator unit.
Blood Separators separate platelets from blood. A bearing is used to to provide rotary fluid exchange between the collection tray & the separator unit.
Capillary leak syndrome is characterized by the escape of blood plasma through capillary walls, from the blood circulatory system to surrounding tissues, muscle compartments, organs or body cavities. It is a phenomenon most commonly witnessed in sepsis, and less frequently in autoimmune diseases, differentiation syndrome, engraftment syndrome, hemophagocytic lymphohistiocytosis, the ovarian hyperstimulation syndrome, viral hemorrhagic fevers, and snakebite and ricin poisoning. Pharmaceuticals, including the chemotherapy medication gemcitabine, as well as certain interleukins and monoclonal antibodies, can also cause capillary leaks. These conditions and factors are sources of secondary capillary leak syndrome. Systemic capillary leak syndrome (SCLS, or Clarksons disease), or primary capillary leak syndrome, is a rare, grave and episodic medical condition observed largely in otherwise healthy individuals mostly in middle age. It is characterized by self-reversing episodes during which the ...
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Abstract: : Purpose: Previously, we demonstrated that Pigment Epithelial Derived Factor (PEDF) blocks VEGF-induced retinal vascular permeability in vivo in a dose dependent manner. Since an increase in VEGF expression and retinal vascular leakage is associated with diabetic retinopathy and diabetic macular edema, we investigated whether exogenously added PEDF could inhibit diabetes-induced retinal vascular permeability. Methods: Retinal vascular leakage in non-diabetic and STZ-induced diabetic Sprague-Dawley rats was measured by the Evans Blue albumin permeation technique. At days 11 and 13 after induction of diabetes, 10 ul of PEDF (200 ng/eye, 40nM final) was injected into one eye and vehicle (0.1% BSA in PBS) was injected into the contralateral eye under sterile conditions. The intact condition of each eye and retina was assessed 24 hours after each injection. At day 14, the animals were sacrificed and retinal vascular permeability was determined. Results: Vascular leakage was increased by ...
Vascular endothelial growth factor is an important signaling protein involved in both vasculogenesis and angiogenesis. As its name implies, VEGF activity has been mostly studied on cells of the vascular endothelium, although it does have effects on a number of other cell types (e.g. stimulation monocyte/macrophage migration, neurons, cancer cells, kidney epithelial cells). VEGF mediates increased vascular permeability, induces angiogenesis, vasculogenesis and endothelial cell growth, promotes cell migration, and inhibits apoptosis. In vitro, VEGF has been shown to stimulate endothelial cell mitogenesis and cell migration. VEGF is also a vasodilator and increases microvascular permeability and was originally referred to as vascular permeability factor. Elevated levels of this protein is linked to POEMS syndrome, also known as Crow-Fukase syndrome. Mutations in this gene have been associated with proliferative and nonproliferative diabetic retinopathy. Human recombinant VEGF-165 produced in yeast ...
in Journal of Pharmacology and Experimental Therapeutics (The) (1994), 270(1), 30-6. The effects of calcitonin gene-related peptide (CGRP) (6 x 10(-8) M) on hemodynamics and on pulmonary microvascular permeability were investigated in isolated, perfused rabbit lungs by measuring the ... [more ▼]. The effects of calcitonin gene-related peptide (CGRP) (6 x 10(-8) M) on hemodynamics and on pulmonary microvascular permeability were investigated in isolated, perfused rabbit lungs by measuring the arterial, capillary and venous pressures and the capillary filtration coefficient (Kf,c). CGRP was administered alone or in combination with capsaicin (10(-4) M), acetylcholine (ACh) (10(-11) M to 10(-7) M), substance P (SP) (10(-10) M to 10(-6) M) and serotonin (10(-4) M). The influence of a specific antagonist of CGRP receptors, CGRP8-37 (10(-8) M), on the pulmonary edema induced by these mediators was also considered. CGRP had no direct effect on the vascular pressures or on Kf,c. Capsaicin and ...
Temperature programmed desorption (TPD) is a method for obtaining information about quantities and binding properties of adsorbed species on a surface. A microfabricated flow system for TPD with an integrated capillary leak to a mass spectrometer is presented. The use of an integrated capillary leak minimizes dead volumes in the system, resulting in increased sensitivity and reduced response time. These properties make the system ideal for TPD experiments in a carrier gas. With CO desorbing from platinum as model system, it is shown that CO desorbing in 105 Pa of argon from as little as 0.5 cm2 of platinum foil gives a clear desorption peak. By using the microfabricated flow system, TPD experiments can be performed in a carrier gas with a sensitivity approaching that of TPD experiments in vacuum. ©2004 American Institute of Physics ...
Trypsin-induced acute inflammation was studied in hamster cheek pouch using intravital microscopy, correlative histology, and electron microscopy. Vascular permeability changes were monitored with intravital fluoroscopy, after intravenous injection of FITC-dextran (Mw 150,000), by counting the number of FITC-dextran leakages around the vessels. The number of extravasated polymorphonuclear leukocytes (PMNLs) was calculated by a histological technique. A dose-dependent increase in the number of FITC-dextran leakages, as well as the number of accumulated PMNLs, was found when trypsin was locally deposited in concentrations of 0.25-2.5 microM (15 microliters during 5 min). Local deposition of autologous serum treated with trypsin at final concentrations of 0.25-2.5 microM caused an increase in vascular permeability as equally pronounced as that of pure trypsin, but only a moderate PMNL accumulation which was not dose dependent. Trypsin at a 25 microM concentration resulted in numerous microbleedings ...
This unit describes various protocols for the in vivo quantitation of drug permeability across the rodent blood ‐ brain barrier
The very interesting review on the systemic capillary leakage of circulating macromolecules (1) suggests capillary dysfunction. An analogous and more common case is renal proteinuria. The heparan sulfate proteoglycan of the glomerular basement membrane is thought to be a key element to retain erythrocytes and plasma protein in circulation. This may be achieved by the negative net charge of the proteoglycans, which repels cells and other protein species ...
BACKGROUND: Blood brain barrier (BBB) disruption is accompanied by edema in the surrounding areas of the intracerebral hemorrhage (ICH). The aim of the study was to clarify the correlation between BBB breakdown and outcome in ICH. PATIENTS: Twenty-se
The endothelial glycocalyx forms a continuous coat over the luminal surface of all vessels, and regulates multiple vascular functions. The contribution of individual components of the endothelial glycocalyx to one critical vascular function, microvascular permeability, remains unclear. We developed novel, real time, paired methodologies to study the contribution of sialic acids within the endothelial glycocalyx to the structural and functional permeability properties of the same microvessel in vivo. Single perfused rat mesenteric microvessels were perfused with fluorescent endothelial cell membrane and glycocalyx labels, and imaged with confocal microscopy. A broad range of glycocalyx depth measurements (0.17-3.02μm) were obtained with different labels, imaging techniques and analysis methods. The distance between peak cell membrane and peak glycocalyx label provided the most reliable measure of endothelial glycocalyx anatomy, correlating with paired, numerically smaller values of endothelial ...
The objective of this study was to assess the impact of CAGB surgery-induced alterations in ANG1, ANG2 and TIE2 levels on post-surgical SIRS and to evaluate potential mechanisms inducing capillary leakage. Our results indicate that CABG induced profound changes in the ANG2/ANG1 balance with loss of the barrier-protective ANG1 and an increase in the barrier-disruptive ANG2 contents in the patients serum. This imbalance was observed in adult patients with systemic pro-inflammatory response characterized by elevated IL-6 levels. The molecular changes correlated with clinical surrogate parameters of an impaired endothelial barrier function, such as fluid balance, application of vasoconstrictors, and prolonged ventilation.. In healthy individuals, constitutive expression of ANG1 results in much higher serum concentrations than ANG2, which is mainly secreted upon endothelial stimulation; therefore, an increased ratio between ANG2 and ANG1 (in healthy adults a numerical value below 1) serves as marker ...
Quantitative MRI reveals the elderly ischemic brain is susceptible to increased early blood-brain barrier permeability following tissue plasminogen activator related to claudin 5 and occludin disassembly
A patient had fatal hypovolemic shock and edema. As in previously reported cases, the mechanism of shock appears to be loss of protein and fluid from the vascul
The Caco-2 permeability assay provides a measure of the permeability of a test compound across the intestinal barrier and its potential for interactions with drug transporters. We provide permeability assays for small molecule formulations such as pharmaceuticals, industrial chemicals and consumer products.
TY - JOUR. T1 - Airway extravasation induced by increasing airway temperature in ovalbumin-sensitized rats. AU - Hsu, Chun-Chun. AU - Tapia, Reyno J.. AU - Lee, Lu-Yuan. N1 - Export Date: 11 May 2016 CODEN: RPNEA 通訊地址: Lee, L.-Y.; Department of Physiology, University of Kentucky Medical Center, 800 Rose St., MS511A, United States 化學物質/CAS: Evans blue, 314-13-6; formoterol, 73573-87-2; ovalbumin, 77466-29-6 參考文獻: Baluk, P., Bolton, P., Hirata, A., Thurston, G., McDonald, D.M., Endothelial gaps and adherent leukocytes in allergen-induced early- and late-phase plasma leakage in rat airways (1998) Am. J. Pathol., 152, pp. 1463-1476; Baluk, P., McDonald, D.M., The beta 2-adrenergic receptor agonist formoterol reduces microvascular leakage by inhibiting endothelial gap formation (1994) Am. J. Physiol., 266, pp. L461-L468; Evans, T.W., Rogers, D.F., Aursudkij, B., Chung, K.F., Barnes, P.J., Inflammatory mediators involved in antigen-induced airway microvascular leakage in guinea ...
Principal Investigator:SHIMADA Yasuhiro, Project Period (FY):1997 - 1999, Research Category:Grant-in-Aid for Scientific Research (B), Section:一般, Research Field:Anesthesiology/Resuscitation studies
Edema can be caused by increased hydrostatic pressure (eg due to venous stasis in the case of varicose veins of the lower limbs), or colloid osmotic pressure reduction (for example due to any disease that results in hypoalbuminemia) significant enough not allow more than the lymphatic vessels to drain fluid that accumulates in the interstitial spaces, inflated. It can be caused by obstruction of the lymphatic vessels, which can no longer drain the interstitial fluid (lymphedema) and excessive sodium retention. In these cases, the liquid that accumulates in the interstitial spaces is called transudate as it has a lower specific gravity was 1.012 kg / m 3, is low in protein and contains no inflammatory cells. Finally, you can have swelling in case of inflammation (inflammatory edema) because it increases vascular permeability. In this case the liquid exudate has accumulated since it has high specific gravity, greater than 1.020kg / m 3, is rich in proteins and inflammatory cells. The swelling ...
Compositions, methods, kits, and apparatus are provided for delivering a macromolecular assembly such as a plasmid, virus vector, or other gene vector, to an extravascular tissue such as muscle tissue. The composition comprises the macromolecular assembly and a vascular permeability-enhancing agent. In another embodiment, the composition further comprises a vasodilating agent. The method of the invention comprises proving a vascular permeability-enhancing agent to a blood vessel and providing a macromolecular assembly to the vessel. An oxygenator useful for providing oxygen to a fluid extracorporeally prior to providing the fluid to a blood vessel of a mammal is included in the invention. Kits, apparatus, and methods for using the catheters described herein for isolating cardiac circulation, diverting caval blood flow from the right atrium, and for other purposes, are also described.