scholarly journals Sphingolipids in Lung Endothelial Biology and Regulation of Vascular Integrity

2013 ◽  
pp. 201-226 ◽  
Author(s):  
Taimur Abbasi ◽  
Joe G. N. Garcia
Keyword(s):  
Vascular Integrity

Non-Thrombogenicity of Clean Glass Revealed by Native Whole Blood Assay in Bead Columns

1983 ◽  
Vol 50 (04) ◽  
pp. 814-820 ◽  
Author(s):  
J A Bergeron ◽  
J M DiNovo ◽  
A F Razzano ◽  
W J Dodds
Keyword(s):  
Whole Blood ◽  
Glass Bead ◽  
Factor Xii ◽  
Platelet Factor ◽  
Serotonin Content ◽  
Whole Blood Assay ◽  
Vascular Integrity ◽  
Blood Assay ◽  
Standard Contact ◽  
Recalcification Time

SummaryThe previously described native whole blood assay for materials in solution or suspension has been adapted to materials in a bead column configuration. These experiments showed that the glass itself accounts for little or none of the high blood-reactivity observed with conventional glass bead columns. Columns composed solely of soft glass that was “cleaned” by heat treatment (500-595° C 18 hr, electric oven) were benign toward flowing native whole blood for all variables measured (platelet count and platelet-free plasma [C14]-serotonin content, platelet factor 3 and factor XII activities, and recalcification time) with the standard contact protocol. In addition, the effluent successfully maintained perfusion of the isolated kidney, a measure of the ability of platelets to support vascular integrity. Prolonged (30 min) normothermic contact with titrated whole blood increased the subsequent reactivity of initially clean glass toward whole blood albeit to a level much less than that of conventional glass bead columns.

High Levels of Serum Hyaluronan Predicts Severe Dengue Infection and Perturbs Vascular Integrity

2019 ◽  
Author(s):  
Chun-Yu Lin ◽  
Constantinos Kolliopoulos ◽  
Chung-Hao Huang ◽  
Jyrki Tenhunen ◽  
Carl-Henrik Heldin ◽  
...  
Keyword(s):  
Dengue Infection ◽  
Severe Dengue ◽  
Vascular Integrity ◽  
Serum Hyaluronan

scholarly journals Vascular Inflammation Is Associated with Loss of Aquaporin 1 Expression on Endothelial Cells and Increased Fluid Leakage in SARS-CoV-2 Infected Golden Syrian Hamsters

Viruses ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 639
Author(s):  
Lisa Allnoch ◽  
Georg Beythien ◽  
Eva Leitzen ◽  
Kathrin Becker ◽  
Franz-Josef Kaup ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Inflammation ◽  
Intercellular Junctions ◽  
Edema Formation ◽  
Vascular Integrity ◽  
Syrian Hamsters ◽  
Aquaporin 1 ◽  
Vascular Walls ◽  
Transmission Electron ◽  
Mock Infection

Vascular changes represent a characteristic feature of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection leading to a breakdown of the vascular barrier and subsequent edema formation. The aim of this study was to provide a detailed characterization of the vascular alterations during SARS-CoV-2 infection and to evaluate the impaired vascular integrity. Groups of ten golden Syrian hamsters were infected intranasally with SARS-CoV-2 or phosphate-buffered saline (mock infection). Necropsies were performed at 1, 3, 6, and 14 days post-infection (dpi). Lung samples were investigated using hematoxylin and eosin, alcian blue, immunohistochemistry targeting aquaporin 1, CD3, CD204, CD31, laminin, myeloperoxidase, SARS-CoV-2 nucleoprotein, and transmission electron microscopy. SARS-CoV-2 infected animals showed endothelial hypertrophy, endothelialitis, and vasculitis. Inflammation mainly consisted of macrophages and lower numbers of T-lymphocytes and neutrophils/heterophils infiltrating the vascular walls as well as the perivascular region at 3 and 6 dpi. Affected vessels showed edema formation in association with loss of aquaporin 1 on endothelial cells. In addition, an ultrastructural investigation revealed disruption of the endothelium. Summarized, the presented findings indicate that loss of aquaporin 1 entails the loss of intercellular junctions resulting in paracellular leakage of edema as a key pathogenic mechanism in SARS-CoV-2 triggered pulmonary lesions.

scholarly journals Polymerized albumin restores impaired hemodynamics in endotoxemia and polymicrobial sepsis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Donald A. Belcher ◽  
Alexander T. Williams ◽  
Andre F. Palmer ◽  
Pedro Cabrales
Keyword(s):  
Septic Shock ◽  
Immune Response ◽  
Fluid Resuscitation ◽  
Cecal Ligation ◽  
Vascular Wall ◽  
Polymicrobial Sepsis ◽  
Vascular Integrity ◽  
Fluid Extravasation ◽  
Inflammatory Immune Response ◽  
Polymerized Human Serum Albumin

AbstractFluid resuscitation following severe inflammation-induced hypoperfusion is critical for the restoration of hemodynamics and the prevention of multiorgan dysfunction syndrome during septic shock. Fluid resuscitation with commercially available crystalloid and colloid solutions only provides transient benefits, followed by fluid extravasation and tissue edema through the inflamed endothelium. The increased molecular weight (M.W.) of polymerized human serum albumin (PolyHSA) can limit fluid extravasation, leading to restoration of hemodynamics. In this prospective study, we evaluated how fluid resuscitation with PolyHSA impacts the hemodynamic and immune response in a lipopolysaccharide (LPS) induced endotoxemia mouse model. Additionally, we evaluated fluid resuscitation with PolyHSA in a model of polymicrobial sepsis induced by cecal ligation and puncture (CLP). Resuscitation with PolyHSA attenuated the immune response and improved the maintenance of systemic hemodynamics and restoration of microcirculatory hemodynamics. This decrease in inflammatory immune response and maintenance of vascular wall shear stress likely contributes to the maintenance of vascular integrity following fluid resuscitation with PolyHSA. The sustained restoration of perfusion, decrease in pro-inflammatory immune response, and improved vascular integrity that results from the high M.W. of PolyHSA indicates that a PolyHSA based solution is a potential resuscitation fluid for endotoxic and septic shock.

scholarly journals Effects of controlled ovarian stimulation on vascular barrier and endothelial glycocalyx: a pilot study

2021 ◽  
Author(s):  
Nikolai Hulde ◽  
N. Rogenhofer ◽  
F. Brettner ◽  
N. C. Eckert ◽  
I. Fetz ◽  
...  
Keyword(s):  
Ovarian Stimulation ◽  
Capillary Permeability ◽  
Serum Levels ◽  
Controlled Ovarian Stimulation ◽  
Endothelial Glycocalyx ◽  
Control Group ◽  
Vascular Integrity ◽  
Fluid Extravasation ◽  
Endothelial Surface ◽  
Infertility Patients

Abstract Purpose Controlled ovarian stimulation significantly amplifies the number of maturing and ovulated follicles as well as ovarian steroid production. The ovarian hyperstimulation syndrome (OHSS) increases capillary permeability and fluid extravasation. Vascular integrity intensely is regulated by an endothelial glycocalyx (EGX) and we have shown that ovulatory cycles are associated with shedding of EGX components. This study investigates if controlled ovarian stimulation impacts on the integrity of the endothelial glycocalyx as this might explain key pathomechanisms of the OHSS. Methods Serum levels of endothelial glycocalyx components of infertility patients (n=18) undergoing controlled ovarian stimulation were compared to a control group of healthy women with regular ovulatory cycles (n=17). Results Patients during luteal phases of controlled ovarian stimulation cycles as compared to normal ovulatory cycles showed significantly increased Syndecan-1 serum concentrations (12.6 ng/ml 6.1125th–19.1375th to 13.9 ng/ml 9.625th–28.975th; p=0.026), indicating shedding and degradation of the EGX. Conclusion A shedding of EGX components during ovarian stimulation has not yet been described. Our study suggests that ovarian stimulation may affect the integrity of the endothelial surface layer and increasing vascular permeability. This could explain key features of the OHSS and provide new ways of prevention of this serious condition of assisted reproduction.

scholarly journals Maintenance of vascular integrity: Role of nitric oxide and other bradykinin mediators

1995 ◽  
Vol 16 (suppl K) ◽  
pp. 4-12 ◽  
Author(s):  
F. Cosentino ◽  
T. F. Luscher
Keyword(s):  
Nitric Oxide ◽  
Vascular Integrity

Platelet Disorders

2015 ◽  
Author(s):  
Lawrence L K Leung ◽  
James L. Zehnder
Keyword(s):  
Platelet Function ◽  
Clinical Manifestations ◽  
Von Willebrand Disease ◽  
Drug Induced ◽  
Excessive Bleeding ◽  
Vascular Integrity ◽  
Patient Reports ◽  
Platelet Function Disorders ◽  
Hemorrhagic Disorders ◽  
Von Willebrand

A bleeding disorder may be suspected when a patient reports spontaneous or excessive bleeding or bruising, often secondary to trauma. Possible causes can vary between abnormal platelet number or function, abnormal vascular integrity, coagulation defects, fibrinolysis, or a combination thereof. This review addresses hemorrhagic disorders associated with quantitative or qualitative platelet abnormalities, such as thrombocytopenia, platelet function disorders, thrombocytosis and thrombocythemia, and vascular purpuras. Hemorrhagic dis­orders associated with abnormalities in coagulation (e.g., von Willebrand disease and hemophilia) are not covered. An algorithm shows evidence-based practice guidelines for the management of immune thrombocytopenic purpura. Tables list questions regarding bleeding and bruising to ask patients, clinical manifestations of hemorrhagic disorders, typical results of tests for hemostatic function in bleeding disorders, causes of thrombocytopenia, other forms of drug-induced thrombocytopenia, classification of platelet function disorders, and selected platelet-modifying agents. This review contains ­1 highly rendered figure, 7 tables, and 82 references. 

Abstract P419: A Systematic Characterization of Brain Endothelial Cell Death in Intracerebral Hemorrhage

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Maulana Ikhsan ◽  
Marietta Zille
Keyword(s):  
Cell Death ◽  
Intracerebral Hemorrhage ◽  
Brain Tissue ◽  
Vascular Integrity ◽  
Regulated Cell Death ◽  
Injury Mechanisms ◽  
Endothelial Cell Death ◽  
Cell Death Mechanisms ◽  
Underlying Mechanisms

Introduction: Intracerebral hemorrhage (ICH) is a type of stroke caused by the loss of vascular integrity leading to bleeding within the brain tissue. Hematoma-derived factors cause secondary injury mechanisms such as cell death days to weeks after the event and in regions distant from the primary insult. Increasing evidence suggests that hemoglobin released by the hematoma is one of the major contributors to neuronal injury in ICH. To date, it is unclear whether brain endothelial cells (EC) are similarly vulnerable to hemolysis products and undergo regulated cell death. Hypothesis: We hypothesized that brain EC undergo multiple, different modes of cell death after ICH and that the underlying mechanisms are different compared to neurons. Methods: We systematically investigated cell death mechanisms in brain EC after exposure to the hemolysis product hemin. We used chemical inhibitors of apoptosis, autophagy, ferroptosis, necroptosis, and parthanatos and assessed biochemical markers of these cell death modes. Results: Brain EC viability was concentration-dependently decreased, starting at higher hemin concentrations than neurons. Treatment of EC with ferroptosis inhibitors protective against hemin toxicity in neurons and against ICH in vivo showed that only N-acetylcysteine and deferoxamine protected brain EC, while ferrostatin-1 and U0126 did not abrogate EC death. The autophagy inhibitor bafilomycin A1 also reduced EC death and hemin increased the expression of the autophagy marker LC3. While inhibitors against apoptosis and parthanatos were not effective, the necroptosis inhibitor GSK872 demonstrated a partial protective effect. Conclusions: Our data suggest that ICH induces different mechanisms of death in EC (ferroptosis and autophagy) compared to neurons (ferroptosis and necroptosis) and may thus warrant a combinatorial therapeutic approach. Further investigations in human and ovine ICH brain tissue are ongoing.

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