scholarly journals The Protective Effects of Statins Towards Vessel Wall Injury Caused by a Stent Retrieving Mechanical Thrombectomy Device : A Histological Analysis of the Rabbit Carotid Artery Model

2021 ◽  
Author(s):  
Seung Hwan Lee ◽  
Hee Sup Shin ◽  
Inho Oh
Keyword(s):  
Carotid Artery ◽  
Vessel Wall ◽  
Histological Analysis ◽  
Mechanical Thrombectomy ◽  
Protective Effects ◽  
Rabbit Carotid Artery ◽  
Thrombectomy Device ◽  
Wall Injury

scholarly journals Transport of Low-Density Lipoprotein Into the Blood Vessel Wall During Atherogenic Diet in the Isolated Rabbit Carotid Artery

2015 ◽  
Vol 79 (8) ◽  
pp. 1846-1852 ◽  
Author(s):  
Maja Colic ◽  
Suzana Pantovic ◽  
Marija Jeremic ◽  
Vuk Jokovic ◽  
Zdravko Obradovic ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Blood Vessel ◽  
Vessel Wall ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Atherogenic Diet ◽  
Low Density ◽  
Blood Vessel Wall ◽  
Rabbit Carotid Artery

scholarly journals Vascular protective effect of aspirin and rivaroxaban upon endothelial denudation of the mouse carotid artery

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
T. G. Mastenbroek ◽  
M. F. A. Karel ◽  
M. Nagy ◽  
W. Chayoua ◽  
E. I. J. Korsten ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Vessel Wall ◽  
Thrombus Formation ◽  
Positive Trend ◽  
Atherosclerotic Cardiovascular Disease ◽  
Protective Effects ◽  
Endothelial Denudation ◽  
Vascular Stiffening

Abstract While in recent trials the dual pathway inhibition with aspirin plus rivaroxaban has shown to be efficacious in patients with atherosclerotic cardiovascular disease, little is known about the effects of this combination treatment on thrombus formation and vascular remodelling upon vascular damage. The aim of this study was to examine the effects of aspirin and/or rivaroxaban on injury-induced murine arterial thrombus formation in vivo and in vitro, vessel-wall remodelling, and platelet-leukocyte aggregates. Temporary ligation of the carotid artery of C57BL/6 mice, fed a western type diet, led to endothelial denudation and sub-occlusive thrombus formation. At the site of ligation, the vessel wall stiffened and the intima-media thickened. Aspirin treatment antagonized vascular stiffening and rivaroxaban treatment led to a positive trend towards reduced stiffening. Local intima-media thickening was antagonized by both aspirin or rivaroxaban treatment. Platelet-leukocyte aggregates and the number of platelets per leukocyte were reduced in aspirin and/or rivaroxaban treatment groups. Furthermore, rivaroxaban restricted thrombus growth and height in vitro. In sum, this study shows vascular protective effects of aspirin and rivaroxaban, upon vascular injury of the mouse artery.

scholarly journals Histological evaluation of acute ischemic stroke thrombi may indicate the occurrence of vessel wall injury during mechanical thrombectomy

2021 ◽  
pp. neurintsurg-2021-017310
Author(s):  
Oana Madalina Mereuta ◽  
Mehdi Abbasi ◽  
Seán Fitzgerald ◽  
Daying Dai ◽  
Ram Kadirvel ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Vessel Wall ◽  
Mechanical Thrombectomy ◽  
Smooth Muscle Actin ◽  
Cerebral Arteries ◽  
Histological Evaluation ◽  
Wall Injury ◽  
Number Of Passes

BackgroundSeveral animal studies have demonstrated that mechanical thrombectomy (MT) for acute ischemic stroke (AIS) may cause vessel wall injury (VWI). However, the histological changes in human cerebral arteries following MT are difficult to determine.ObjectiveTo investigate the occurrence of VWI during MT by histological and immunohistochemical evaluation of AIS clots.MethodsAs part of the multicenter STRIP registry, 277 clots from 237 patients were analyzed using Martius Scarlett Blue stain and immunohistochemistry for CD34 (endothelial cells) and smooth muscle actin (smooth muscle cells).ResultsMT devices used were aspiration catheters (100 cases), stentriever (101 cases), and both (36 cases). VWI was found in 33/277 clots (12%). There was no significant correlation between VWI and MT device. The degree of damage varied from grade I (mild intimal damage, 24 clots), to grade II (relevant intimal and subintimal damage, 3 clots), and III (severe injury, 6 clots). VWI clots contained significantly more erythrocytes (p=0.006*) and less platelets/other (p=0.005*) than non-VWI clots suggesting soft thrombus material.Thrombolysis correlated with a lower rate of VWI (p=0.04*). VWI cases showed a significantly higher number of passes (2 [1–4] vs 1 [1–3], p=0.028*) and poorer recanalization outcome (p=0.01*) than cases without VWI.ConclusionsHistological markers of VWI were present in 12% of AIS thrombi, suggesting that VWI might be related to MT. VWI was associated with soft thrombus consistency, higher number of passes and poorer revascularization outcome. There was no significant correlation between VWI and MT device.

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.

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