scholarly journals Arginine reduces leukocyte/endothelial cell interaction in a model of normotensive endotoxemia without attenuating capillary perfusion failure

Critical Care ◽  
2008 ◽  
Vol 12 (Suppl 2) ◽  
pp. P147
Author(s):  
J Fertmann ◽  
M Laschke ◽  
B Vollmar ◽  
MD Menger ◽  
JN Hoffmann
Keyword(s):  
Endothelial Cell ◽  
Cell Interaction ◽  
Capillary Perfusion ◽  
Endothelial Cell Interaction ◽  
Perfusion Failure

Antithrombin reduces leukocyte adhesion during chronic endotoxemia by modulation of the cyclooxygenase pathway

2000 ◽  
Vol 279 (1) ◽  
pp. C98-C107 ◽  
Author(s):  
J. N. Hoffmann ◽  
B. Vollmar ◽  
D. Inthorn ◽  
F. W. Schildberg ◽  
M. D. Menger
Keyword(s):  
Endothelial Cell ◽  
Leukocyte Adhesion ◽  
Repeated Administration ◽  
Capillary Density ◽  
Cell Interaction ◽  
Multiple Organ ◽  
Microvascular Perfusion ◽  
Leukocyte Adherence ◽  
Capillary Perfusion ◽  
Endothelial Cell Interaction

Antithrombin (AT) is known as the most important natural inhibitor of thrombin activity and has been shown to improve distinct clinical parameters during the course of septic (endotoxin)-induced multiple organ dysfunction. We hypothesized that AT acts by inhibiting leukocyte activation and microvascular injury via the promotion of endothelial release of PGI2, and therefore, we studied the effects of AT on leukocyte/endothelial cell interaction and microvascular perfusion during endotoxemia. In a skinfold preparation of Syrian hamsters, severe endotoxemia was induced by repeated administration of endotoxin intravenously [lipopolysaccharide (LPS), Escherichia coli, 2 mg/kg] at 0 and 48 h. AT (250 IU/kg) was administered intravenously at 0, 24, and 48 h ( n = 6, AT group). In control animals ( n = 5, control), LPS was given without AT supplementation. By intravital fluorescence microscopy, leukocyte-endothelial cell interaction and functional capillary density (FCD; measure of capillary perfusion) were analyzed during a 72-h period after the first LPS injection. AT significantly attenuated LPS-induced arteriolar and venular leukocyte adherence after both the first and the second LPS injection [ P < 0.01, measures analysis of variance (MANOVA)]. In parallel, AT was effective in preventing LPS-induced depression of FCD after the first and the second LPS administration ( P < 0.05, MANOVA). By pretreatment with the cyclooxygenase inhibitor indomethacin ( n = 6), effects of AT on leukocyte adherence and FCD were found completely abolished. Thus our study indicates that AT exerts its beneficial effects in endotoxemia by reducing leukocyte-endothelial cell interaction and microvascular perfusion failure probably via liberation of prostacyclin from endothelial cells.

THE THROMBIN ANTAGONIST HIRUDIN FAILS TO INHIBIT ENDOTOXIN-INDUCED LEUKOCYTE/ENDOTHELIAL CELL INTERACTION AND MICROVASCULAR PERFUSION FAILURE

Shock ◽  
2000 ◽  
Vol 14 (5) ◽  
pp. 528-534 ◽  
Author(s):  
Johannes N. Hoffmann ◽  
Brigitte Vollmar ◽  
Dietrich Inthorn ◽  
Friedrich W. Schildberg ◽  
Michael D. Menger
Keyword(s):  
Endothelial Cell ◽  
Cell Interaction ◽  
Microvascular Perfusion ◽  
Endothelial Cell Interaction ◽  
Perfusion Failure

scholarly journals Human recombinant erythropoietin protects the striated muscle microcirculation of the dorsal skinfold from postischemic injury in mice

2007 ◽  
Vol 293 (1) ◽  
pp. H274-H283 ◽  
Author(s):  
Claudio Contaldo ◽  
Christoph Meier ◽  
Ahmed Elsherbiny ◽  
Yves Harder ◽  
Otmar Trentz ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Striated Muscle ◽  
Ischemia Reperfusion ◽  
Cell Interaction ◽  
Sham Operation ◽  
Recombinant Erythropoietin ◽  
Capillary Perfusion ◽  
Early Reperfusion ◽  
Endothelial Cell Interaction ◽  
Late Reperfusion

Erythropoietin (EPO) has been proposed as a novel cytoprotectant in ischemia-reperfusion (I/R) injury of the brain, heart, and kidney. However, whether EPO exerts its protection by prevention of postischemic microcirculatory deterioration is unknown. We have investigated the effect of EPO on I/R-induced microcirculatory dysfunctions. We used the mouse dorsal skinfold chamber preparation to study nutritive microcirculation and leukocyte-endothelial cell interaction in striated muscle of the dorsal skinfold by in vivo fluorescence microscopy before 3 h of ischemia and during 5 days of reperfusion. Animals were pretreated with EPO (5,000 U/kg body wt) 1 or 24 h before ischemia. Vehicle-treated I/R-injured animals served as controls. Additional animals underwent sham operation only or were pretreated with EPO but not subjected to I/R. I/R significantly ( P < 0.05) reduced functional capillary density, increased microvascular permeability, and enhanced venular leukocyte-endothelial cell interaction during early reperfusion. These findings were associated with pronounced ( P < 0.05) arteriolar constriction and diminution of blood flow during late reperfusion. Pretreatment with EPO induced EPO receptor and endothelial nitric oxide synthase expression at 6 h of reperfusion ( P < 0.05). In parallel, EPO significantly ( P < 0.05) reduced capillary perfusion failure and microvascular hyperpermeability during early reperfusion and arteriolar constriction and flow during late reperfusion. EPO pretreatment substantially ( P < 0.05) diminished I/R-induced leukocytic inflammation by reducing the number of rolling and firmly adhering leukocytes in postcapillary venules. EPO applied 1 h before ischemia induced angiogenic budding and sprouting at 1 and 3 days of reperfusion and formation of new capillary networks at 5 days of reperfusion. Thus our study demonstrates for the first time that EPO effectively attenuates I/R injury by preserving nutritive perfusion, reducing leukocytic inflammation, and inducing new vessel formation.

In Vivo Assessment of Synovial Microcirculation and Leukocyte–Endothelial Cell Interaction in Mouse Antigen-Induced Arthritis

1999 ◽  
Vol 6 (4) ◽  
pp. 281-290 ◽  
Author(s):  
A N D R E A S VEIHELMANN ◽  
ANTHONY G U S T A V E HARRIS ◽  
F R I T Z KROMBACH ◽  
E L K E SCHÜTZE ◽  
HANS JÜRGEN REFIOR ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Interaction ◽  
Endothelial Cell Interaction ◽  
In Vivo Assessment

A New Model for Quantitative In Vivo Microscopic Analysis of Thrombus Formation and Vascular Recanalisation: The Ear of the Hairless (hr/hr) Mouse

1997 ◽  
Vol 78 (05) ◽  
pp. 1408-1414 ◽  
Author(s):  
Frank Roesken ◽  
Martin Ruecker ◽  
Brigitte Vollmar ◽  
Nicole Boeckel ◽  
Eberhard Morgenstern ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Light Exposure ◽  
Thrombus Formation ◽  
Microscopic Analysis ◽  
Cell Interaction ◽  
Vascular Perfusion ◽  
Vessel Occlusion ◽  
Endothelial Cell Interaction ◽  
Platelet Deposition

SummaryThe alteration of rheological blood properties as well as deterioration of vascular perfusion conditions and cell-cell interactions are major determinants of thrombus formation. Herein, we present an experimental model which allows for quantitative in vivo microscopic analysis of these determinants during both thrombus formation and vascular recanalisation. The model does not require surgical preparation procedures, and enables for repeated analysis of identical microvessels over time periods of days or months, respectively. After i.v. administration of FITC-dextran thrombus formation was induced photochemically by light exposure to individual arterioles and venules of the ear of ten anaesthetised hairless mice. In venules, epiillumination induced rapid thrombus formation with first platelet deposition after 0.59 ± 0.04 min and complete vessel occlusion within 7.48 ±1.31 min. After a 24-h time period, 75% of the thrombosed venules were found recanalised. Marked leukocyte-endothelial cell interaction in those venules indicated persistent endothelial cell activation and/or injury, even after an observation period of 7 days. In arterioles, epi-illumination provoked vasomotion, while thrombus formation was significantly (p <0.05) delayed with first platelet deposition after 2.32 ± 0.22 min and complete vessel occlusion within 20.07 ±3.84 min. Strikingly, only one of the investigated arterioles was found recanalised after 24 h, which, however, did not show leukocyte-endothelial cell interaction. Heparin (300 U/kg, i.v.) effectively counteracted the process of thrombus formation in this model, including both first platelet deposition and vessel occlusion. We conclude that the model of the ear of the hairless mouse allows for distinct in vivo analysis of arteriolar and venular thrombus formation/ recanalisation, and, thus, represents an interesting tool for the study of novel antithrombotic and thrombolytic strategies, respectively.

Integrated Microfluidic Platform with Multiple Functions To Probe Tumor–Endothelial Cell Interaction

2017 ◽  
Vol 89 (18) ◽  
pp. 10037-10044 ◽  
Author(s):  
Ling Lin ◽  
Xuexia Lin ◽  
Luyao Lin ◽  
Qiang Feng ◽  
Takehiko Kitamori ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Interaction ◽  
Microfluidic Platform ◽  
Multiple Functions ◽  
Endothelial Cell Interaction ◽  
Tumor Endothelial Cell

Pericyte–endothelial cell interaction increases MMP-9 secretion at the blood–brain barrier in vitro

2008 ◽  
Vol 1189 ◽  
pp. 1-11 ◽  
Author(s):  
Alla Zozulya ◽  
Christian Weidenfeller ◽  
Hans-Joachim Galla
Keyword(s):  
Endothelial Cell ◽  
Blood Brain Barrier ◽  
Cell Interaction ◽  
Brain Barrier ◽  
Endothelial Cell Interaction ◽  
Blood Brain

Tumor-endothelial cell interaction in an experimental model of human hepatocellular carcinoma

2018 ◽  
Vol 372 (1) ◽  
pp. 16-24 ◽  
Author(s):  
Azemat Jamshidi-Parsian ◽  
Robert J. Griffin ◽  
Rajshekhar A. Kore ◽  
Valentina K. Todorova ◽  
Issam Makhoul
Keyword(s):  
Hepatocellular Carcinoma ◽  
Endothelial Cell ◽  
Experimental Model ◽  
Cell Interaction ◽  
Human Hepatocellular Carcinoma ◽  
Endothelial Cell Interaction ◽  
Tumor Endothelial Cell
Sign in / Sign up

Export Citation Format

Share Document