Gene Induction in Vessel Wall Injury

1993 ◽  
Vol 70 (01) ◽  
pp. 180-183 ◽  
Author(s):  
Mark B Taubman
Keyword(s):  
Vessel Wall ◽  
Gene Induction ◽  
Wall Injury

The Effects of Heparin and Annexin V on Fibrin Accretion after Injury in the Jugular Veins of Rabbits

1993 ◽  
Vol 69 (03) ◽  
pp. 227-230 ◽  
Author(s):  
J Van Ryn-McKenna ◽  
H Merk ◽  
T H Müller ◽  
M R Buchanan ◽  
W G Eisert
Keyword(s):  
Vessel Wall ◽  
Thrombin Generation ◽  
Antithrombin Iii ◽  
Specific Effect ◽  
Annexin V ◽  
Inhibitory Effect ◽  
Jugular Veins ◽  
Prothrombinase Complex ◽  
Wall Injury

SummaryWe compared the relative abilities of unfractionated heparin and annexin V to prevent fibrin accretion onto injured jugular veins in vivo. Heparin was used to accelerate the inhibition of thrombin by antithrombin III, and annexin V was used to inhibit the assembly of the prothrombinase complex on phospholipid surfaces, thereby blocking thrombin generation. Rabbit jugular veins were isolated in situ, a 2 cm segment was injured by perfusing it with air, and then blood flow was re-established. Five minutes later, each rabbit was injected with heparin (20 U/kg) or annexin V (0.3 mg/kg) and then with 125I-fibrinogen. The amount of 125I-fibrin accumulation onto each injured vessel wall segment was measured 4 h later. Each injured vessel was completely deendothelialized as a result of the air perfusion as demonstrated by electron microscopy. 125I-fibrin accretion onto the injured jugular veins was enhanced 2.4-fold as compared to the uninjured veins in sham-operated animals. Heparin treatment did not reduce fibrin accretion, whereas, annexin V treatment decreased fibrin accretion by 60%, p <0.05. This latter effect was achieved without sustained circulating anticoagulation. Additional experiments confirmed that the inhibitory effect of annexin V on fibrin accretion was associated with a surface specific effect, since more annexin V bound to the injured jugular vein segments as compared to the non-injured jugular veins. We conclude that, i) mild vessel wall injury (selective de-endothelialization) in veins results in a thrombogenic vessel wall; ii) the thrombogenecity of which is not inhibited by prophylactic doses of heparin; but iii) is inhibited by annexin V, which binds to injured vessel wall surface, and inhibits thrombin generation independently of antithrombin III.

scholarly journals Intracranial Arterial Dissection Related to HIV Infection

2005 ◽  
Vol 11 (4) ◽  
pp. 387-391 ◽  
Author(s):  
D. Lefeuvre ◽  
L. Liebenberg ◽  
A. Taylor
Keyword(s):  
Human Immunodeficiency Virus ◽  
Subarachnoid Haemorrhage ◽  
Vessel Wall ◽  
False Aneurysm ◽  
Hiv Positive ◽  
Pathological Study ◽  
Hiv Virus ◽  
Immunodeficiency Virus ◽  
The Right ◽  
Wall Injury

There are many reasons for patients infected with human immunodeficiency virus (HIV) to develop cerebrovascular disease. The HIV virus itself however may be a cause of vessel wall pathology. We present a clinical and pathological study of a patient who was HIV positive and presented with a subarachnoid haemorrhage. Cerebral angiography and later histology confirm that there was extensive vessel wall injury with dissection and a false aneurysm of the right middle cerebral artery.

scholarly journals 211 MRI of coronary vessel wall injury in a swine model of coronary intervention using an eletrostatically stabilized VSOP nanoparticle

2008 ◽  
Vol 10 (Suppl 1) ◽  
pp. A72 ◽  
Author(s):  
Christian von Bary ◽  
Anne Preissel ◽  
Susanne Wagner ◽  
Marcus R Makowski ◽  
Alexandra Keithahn ◽  
...  
Keyword(s):  
Vessel Wall ◽  
Coronary Intervention ◽  
Coronary Vessel ◽  
Swine Model ◽  
Coronary Vessel Wall ◽  
Wall Injury

Effects of Antisense c- myb Oligonucleotides on Vascular Smooth Muscle Cell Proliferation and Response to Vessel Wall Injury

1995 ◽  
Vol 76 (4) ◽  
pp. 505-513 ◽  
Author(s):  
Augusto E. Villa ◽  
Luis A. Guzman ◽  
Earl J. Poptic ◽  
Vinod Labhasetwar ◽  
Stanley D’Souza ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Vessel Wall ◽  
Smooth Muscle Cell Proliferation ◽  
Wall Injury

scholarly journals Resveratrol-Coated Balloon Catheters in Porcine Coronary and Peripheral Arteries

2019 ◽  
Vol 20 (9) ◽  
pp. 2285
Author(s):  
Stefanie Kamann ◽  
Tobias Haase ◽  
Nicola Stolzenburg ◽  
Melanie Löchel ◽  
Daniel Peters ◽  
...  
Keyword(s):  
Vessel Wall ◽  
Inflammatory Responses ◽  
Coronary Vessels ◽  
Peripheral Arteries ◽  
Beneficial Effects ◽  
Balloon Catheters ◽  
Endothelial Denudation ◽  
Vascular Dilatation ◽  
Wall Injury ◽  
Drug Coated Balloon

Angioplasty aiming at vascular dilatation causes endothelial denudation and induces complex inflammatory responses that affect vascular healing, including delayed reendothelialization and excessive neointima proliferation. Resveratrol is known for multiple beneficial effects on the vessel wall after systemic treatment or sustained release from a stent. It is also used as an additive on drug-coated balloon catheters (DCB). In this study, the effect of a single dose of resveratrol, three days to four weeks after administration as a balloon coating during angioplasty, was investigated. Sixteen pigs underwent angioplasty with resveratrol-coated or uncoated balloon catheters in coronary and peripheral arteries. Vessels were overstretched by approximately 20% to enhance vessel wall injury and to produce persistent vessel wall irritation. A significantly reduced number of micro vessels and macrophages in the adventitia, as well as an improved reendothelialization of the vessel lumen, were observed in resveratrol-treated peripheral arteries. The coronaries had a much higher injury score compared to peripheral vessels. Resveratrol-dependent reduction of macrophages, micro vessels or acceleration of reendothelialization was not evident in the coronary vessels. Additionally, no significant effect on neointima proliferation and inflammation score in either vessel territory was observed as a result of resveratrol treatment. In conclusion, the results suggest that resveratrol diminishes the inflammatory response and promotes vascular healing in peripheral arteries. These same effects are absent in more severely injured coronary arteries.

RHEOLOGY AND PRIMARY HEMOSTASIS

1987 ◽  
Author(s):  
F E Grabowski
Keyword(s):  
Endothelial Cell ◽  
Vessel Wall ◽  
Platelet Adhesion ◽  
Cell Monolayer ◽  
Shear Rates ◽  
Primary Hemostasis ◽  
Flowing Blood ◽  
A Site ◽  
Wall Injury ◽  
Oral Aspirin

Overview The adhesion-aggregation of platelets to a site of vessel wall injury is a quintessential blood flow phenomenon. Firstly, platelets are driven to the vicinity of the vessel wall by a form of convective diffusion in which red cells both mechanically augment the effective platelet diffusivity (Turitto et al., Ind. Eng. Chem. Fund. 11:216-223, 1972; Grabowski et al., Ind. Eng. Chem. Fund. 11:224-232, 1972) and enhance the near-wall piatelet concentration (Ti11es and Eckstein, Microvasc Res., In press, 1987). Secondly, red cells subjected to physiologic shear forces are capable of secreting sufficient adenine nucleotides to induce primary platelet aggregation without themselves undergoing frank lysis (Reimers et al, Blood 64:1200-1206, 1984). This "humoral" effect of erythrocytes is likely to contribute to primary hemostasis in a shear stress-dependent manner. Thirdly, endothelial cells are able to modulate platelet aggregation at a site of vessel injury by producing prostacyclin (and perhaps other antithrombotic substances) in a manner which increases with vessel shear rate (Grabowski et al, Blood 62:301a, 1983); production for a large range of arterial shear rates appears to be limited by plasma-borne substrate (arachidonate). This manner of production ensures a concentration of prostacyclin in the near-wall region which remains relatively independent of shear rate.Imaging primary hemostasis. In our work, epi-fluorescence videomicroscopy has allowed real time imaging of platelet adhesion-aggregation to a simulated vessel wall injury. The injury model is an endothelial cell monolayer (ECM) across which, prior to ECM exposure to flowing blood, a 6-0 sterile suture is drawn in a direction transverse to flow. Microinjuries result which measure 70 ± 15μm (Mean ± SD) in width. The fluorescent label is the TAB murine monoclonal antibody (courtesy of Dr. R.P. McEver) directed against human platelet GPIIB, together with a fluorescein-conjugated goat F(ab')2 against murine inmunoglobulin. The injured ECM's, grown to confluence on rectangular cover glasses precoated with microfibrillar collagen, comprise one wall of a flow chamber mounted on a vertical microscope stage. On microinjury sites and at shear rates of 100 to 700 sec-1, computer-enhanced video images show adherence, remodelling and growth of chains of platelet aggregates. Aligned with the flow direction, these chains have a spacing of approximately 30)im, a length similar to the average endothelial cell diameter. One may speculate that such chains provide a scaffold for wound healing insofar as they are likely rich in agents chemotactic for leukocytes and in platelet-derived growth factor.Modulatory role of endothelium. When the ECM's are pre treated with 1.0 mM FC lysine acetyl sal icy late (LA), aggregate length increases (P<0.001) up totwo-fold, outflow levels by RIA of serum thromboxane B2 increase (8 of 8 paired runs), and outflow levels of prostacyclin by RIA for 6-Keto PGFiot decrease (5 of 7 paired runs). The Table gives data for one of four similar experiments at 270 sec-1 and following five minutes of flow. These data imply that products of ECM which are inhibitable by aspirin modulate local adhesion-aggregation; their inhibition, as by vasculitis or drugs, may give rise to thrombotic states.Bleeding disorders. Aggregate length is reduced in von Willebrand's disease (4 patients), Hermansky-Pudlak syndrome (2 patients), and after 300 mg oral aspirin (Tablet 4 donors). The reduction in the first two, however, is greater (P<0.01) than that for oral aspirin. With oral aspirin, further, there is a paradoxic increase in the percent platelet coverage of the injury area. Summary. Rheology has profound effects on the rate, structure, and modulation of primary hemostasis. Many of these effects can be studied via real-time, epi-fluorescence videomicroscopy of platelet adhesion-aggregation to a site of injury to an endothelial cell monolayer exposed to flowing blood. The model described has application to the study of thrombotic and hemostatic disorders and unstable angina.

scholarly journals Antiadhesive effect of fibrinogen: a safeguard for thrombus stability

Blood ◽  
2006 ◽  
Vol 109 (4) ◽  
pp. 1541-1549 ◽  
Author(s):  
Valeryi K. Lishko ◽  
Timothy Burke ◽  
Tatiana Ugarova
Keyword(s):  
Wound Healing ◽  
Vessel Wall ◽  
Potent Inhibitor ◽  
Leukocyte Adhesion ◽  
Fibrin Clot ◽  
Flow Conditions ◽  
High Concentration ◽  
Fibrin Gel ◽  
Wall Injury

Abstract The recruitment of phagocytic leukocytes to sites of vessel wall injury plays an important role in thrombus dissolution by proteases elaborated on their adhesion. However, leukocyte adhesion to the fibrin clot can be detrimental at the early stages of wound healing when hemostatic plug integrity is critical for preventing blood loss. Adhesion of circulating leukocytes to the insoluble fibrin(ogen) matrix is mediated by integrins and occurs in the presence of a high concentration of plasma fibrinogen. In this study, the possibility that soluble fibrinogen could protect fibrin from excessive adhesion of leukocytes was examined. Fibrinogen was a potent inhibitor of adhesion of U937 monocytoid cells and neutrophils to fibrin gel and immobilized fibrin(ogen). An investigation of the mechanism by which soluble fibrinogen exerts its influence on leukocyte adhesion indicated that it did not block integrins but rather associated with the fibrin(ogen) substrate. Consequently, leukocytes that engage fibrinogen molecules loosely bound to the surface of fibrin(ogen) matrix are not able to consolidate their grip on the substrate; subsequently, cells detach. This conclusion is based on the evidence obtained in adhesion studies using various cells and performed under static and flow conditions. These findings reveal a new role of fibrinogen in integrin-mediated leukocyte adhesion and suggest that this mechanism may protect the thrombus from premature dissolution.

Intimatan Prevents Arterial and Venous Thrombosis in a Canine Model of Deep Vessel Wall Injury

2002 ◽  
Vol 301 (3) ◽  
pp. 1151-1156 ◽  
Author(s):  
James K. Hennan ◽  
Ting-Ting Hong ◽  
Ardamanpal K. Shergill ◽  
Edward M. Driscoll ◽  
Alan D. Cardin ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Vessel Wall ◽  
Canine Model ◽  
Wall Injury

A Computational Analysis of an In Vitro Vessel Wall Injury Model

2012 ◽  
Vol 40 (7) ◽  
pp. 1486-1494
Author(s):  
Connie L. Hall ◽  
Fowzia S. Zaman
Keyword(s):  
Vessel Wall ◽  
Computational Analysis ◽  
Injury Model ◽  
Wall Injury
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