CD11b/CD18 as a Marker of Neutrophil Adhesion in Experimental Venous Hypertension

1995 ◽  
pp. 220-221 ◽  
Author(s):  
D. A. Shields ◽  
S. K. Andaz ◽  
C. A. Timothy-Antoine ◽  
J. H. Scurr ◽  
J. B. Porter
VASA ◽  
2014 ◽  
Vol 43 (1) ◽  
pp. 47-54 ◽  
Author(s):  
Weibin Huang ◽  
Weiwei Qin ◽  
Lei Lv ◽  
Haoyv Deng ◽  
Hao Zhang ◽  
...  

Background: Duffy antigen / receptor for chemokines (DARC) possesses high affinity for several chemokine subgroups of CC and CXC. Although DARC has been shown to play a role in many inflammatory diseases, its effect on chronic venous disease (CVD) remains unidentified. We explored whether the expression of DARC in skin tissue was activated under venous hypertension as well as the relationships between DARC and inflammation. Materials and methods: The inflammation in a rat model of venous hypertension caused by a femoral arterial-venous fistula (AVF) was studied. At specified intervals the pressure in the femoral veins was recorded within 42 days. Hindlimb skin specimens were harvested at different time points. The expressions of DARC, interleukin-8 (IL-8), and monocyte chemotactic protein-1 (MCP-1) in skin tissue were examined. Mononuclear cells infiltrated in skin tissue were detected. Results: Femoral venous pressures in AVF groups increased significantly at different time points (P < 0.01). DARC was expressed in skin tissue and its expression level increased significantly in AVF groups from the 7nd day on and was enhanced in a time-dependent manner within 42 days (P < 0.05). Meanwhile, both MCP-1 and IL-8 had higher levels, accompanied by increased mononuclear cells infiltrating into skin tissue (P < 0.05). Conclusions: A rat AVF model which can maintain venous hypertension for at least 42 days is competent for researching the pathogenesis of CVD. DARC, which plays a role in the inflammation of skin tissue under venous hypertension, may become a new molecular target for diagnosis and treatment of CVD at a very early stage.


2000 ◽  
Vol 7 (1) ◽  
pp. 41-52 ◽  
Author(s):  
S H I N Y A TAKASE ◽  
L A U R A N C E LEROND ◽  
JOHN J BERGAN ◽  
GEERT W SCHMID-SCHÖNBEIN

Phlebologie ◽  
2008 ◽  
Vol 37 (05) ◽  
pp. 259-265 ◽  
Author(s):  
H. Kutzner ◽  
G. Hesse

SummaryThe reason of the so called ulcerated capillaritis alba or idiopathic atrophie blanche is vasculopathy caused by severe venous hypertension. Thrombosed and rarificated vessels worsen the oxygenation, increase permanent inflammation and impede the necessary compression therapy. The anti-inflammatory effects of heparin alleviate pain and being independent from the antithrombotic ones it needs much lower doses for treatment. This anti-inflammatory effect is now becoming more important in clinical phlebology. Case studies of more than 50 patients and one prospective randomized study of 87 patients clearly demonstrate the ameliorated healing of ulcerated atrophie blanche. In our office we could document this positive effect with 22 patients. We present the pathophysiology of low molecular heparins for ulcerated capillaritis alba and our own experiences with it.


1992 ◽  
Vol 68 (03) ◽  
pp. 321-324 ◽  
Author(s):  
Irena Keber ◽  
Dušan Keber ◽  
Mojca Stegnar ◽  
Nina Vene

SummaryIn order to study the effects of chronic venous hypertension due to heart failure on blood fibrinolytic activity, tissue plasminogen activator (t-PA) antigen, plasminogen activator inhibitor 1 (PAI-1) antigen, t-PA activity and PAI activity were measured before and after venous occlusion of the arm for 20 min in 15 patients with right-sided heart failure, 15 patients with left-sided heart failure, and 30 control healthy subjects. Central venous pressure, measured by observing the jugular veins, was above 15 cm of the blood column in all patients with right-sided heart failure, and normal (below 8 cm) in all patients with left-sided heart failure and control subjects. There was no difference in the basal concentrations of t-PA (11.0, 10.2 and 10.8 ng/ml; all values medians) and PAI-1 antigens and their activities between right and left-sided heart failure and the control subjects. After the occlusion, t-PA antigen increased significantly less in right-sided heart failure (28.6 ng/ml) than in left-sided heart failure and the control subjects (54.5 and 45.9 ng/ml, respectively). It was concluded that the poor increase in fibrinolytic activity that had already been reported in patients with heart failure, was due to low t-PA release during occlusion and not to a high basal PAI level. It was limited to the patients with right-sided heart failure and was probably the consequence of chronic systemic venous hypertension.


Author(s):  
Mizuko Osaka ◽  
Michiyo Deushi ◽  
Jiro Aoyama ◽  
Tomoko Funakoshi ◽  
Akihito Ishigami ◽  
...  

2021 ◽  
Vol 4 (1) ◽  
pp. 81-83
Author(s):  
Sharath Kumar Goddu Govindappa ◽  
Lakshminarayanapuram Gopal Viswanathan ◽  
Shashidhar Kallappa Parameshwarappa ◽  
Naveen Nayak ◽  
Sujit Kumar ◽  
...  

Intracerebral hemorrhage is a devastating form of stroke and is more common in patients with hypertension and renal disease. We present the case of a lady suffering from chronic kidney disease who presented with severe headache and aphasia. On evaluation, she was found to have an intraparenchymal hemorrhage in the left temporal lobe with prominent pial and dural veins suggestive of a dural arteriovenous fistula (DAVF). Subsequently, she was detected to have occlusion of the left brachiocephalic vein (LBCV), which resulted in venous hypertension and resulted in this rare complication. Angioplasty followed by stenting of the LBCV resulted in subsidence of her symptoms. We wish to highlight this unusual but treatable complication of limb AV fistula which can mimic intracranial DAVF.


2021 ◽  
Vol 10 (15) ◽  
pp. 3239
Author(s):  
Miguel A. Ortega ◽  
Oscar Fraile-Martínez ◽  
Cielo García-Montero ◽  
Miguel A. Álvarez-Mon ◽  
Chen Chaowen ◽  
...  

Chronic venous disease (CVD) is a multifactorial condition affecting an important percentage of the global population. It ranges from mild clinical signs, such as telangiectasias or reticular veins, to severe manifestations, such as venous ulcerations. However, varicose veins (VVs) are the most common manifestation of CVD. The explicit mechanisms of the disease are not well-understood. It seems that genetics and a plethora of environmental agents play an important role in the development and progression of CVD. The exposure to these factors leads to altered hemodynamics of the venous system, described as ambulatory venous hypertension, therefore promoting microcirculatory changes, inflammatory responses, hypoxia, venous wall remodeling, and epigenetic variations, even with important systemic implications. Thus, a proper clinical management of patients with CVD is essential to prevent potential harms of the disease, which also entails a significant loss of the quality of life in these individuals. Hence, the aim of the present review is to collect the current knowledge of CVD, including its epidemiology, etiology, and risk factors, but emphasizing the pathophysiology and medical care of these patients, including clinical manifestations, diagnosis, and treatments. Furthermore, future directions will also be covered in this work in order to provide potential fields to explore in the context of CVD.


1999 ◽  
Vol 277 (3) ◽  
pp. L465-L471 ◽  
Author(s):  
Alessandro Celi ◽  
Silvana Cianchetti ◽  
Stefano Petruzzelli ◽  
Stefano Carnevali ◽  
Filomena Baliva ◽  
...  

Intercellular adhesion molecule-1 (ICAM-1) is the only inducible adhesion receptor for neutrophils identified in bronchial epithelial cells. We stimulated human airway epithelial cells with various agonists to evaluate whether ICAM-1-independent adhesion mechanisms could be elicited. Phorbol 12-myristate 13-acetate (PMA) stimulation of cells of the alveolar cell line A549 caused a rapid, significant increase in neutrophil adhesion from 11 ± 3 to 49 ± 7% (SE). A significant increase from 17 ± 4 to 39 ± 6% was also observed for neutrophil adhesion to PMA-stimulated human bronchial epithelial cells in primary culture. Although ICAM-1 expression was upregulated by PMA at late time points, it was not affected at 10 min when neutrophil adhesion was already clearly enhanced. Antibodies to ICAM-1 had no effect on neutrophil adhesion. In contrast, antibodies to the leukocyte integrin β-chain CD18 totally inhibited the adhesion of neutrophils to PMA-stimulated epithelial cells. These results demonstrate that PMA stimulation of human airway epithelial cells causes an increase in neutrophil adhesion that is not dependent on ICAM-1 upregulation.


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