Accumulation of radiolabelled platelets and fibrin on the carotid artery of rabbits after angioplasty: effects of heparin and dipyridamole

2003 ◽  
Vol 90 (12) ◽  
pp. 1179-1186 ◽  
Author(s):  
Martin Lorenz ◽  
Herbert Merk ◽  
Michael Buchanan ◽  
Wolfgang Eisert ◽  
Joanne van Ryn
Keyword(s):  
Carotid Artery ◽  
Intravenous Infusion ◽  
Vessel Wall ◽  
Carotid Arteries ◽  
Balloon Injury ◽  
Platelet Accumulation ◽  
Measurement Period

SummaryWe investigated the dynamic accumulation of platelets and fibrin after balloon injury of the carotid arteries in rabbits in vivo. In addition, effects of heparin and dipyridamole treatment were also tested. Autologous 99mTc-labelled platelet and 123I-labelled fibrin accumulation was measured at one minute intervals for 4 hours following balloon injury of the carotid artery. Platelet accumulation occurred rapidly, with a ~125% increase occurring within 30 min after injury. There was no further activity for up to 4 hours. This accumulation could be inhibited with an intravenous infusion of PGI2 (500 ng/kg/hr). Fibrin accumulation occurred slowly and continuously over the 4 hour measurement period. Injection of an anti-fibrin antibody inhibited fibrin accumulation. Heparin (25 U/kg/hr for 4 hrs) administration resulted in a significant 82 ± 19% and 68 ± 13% reduction in platelet and fibrin accumulation, respectively. This dose of heparin was associated with a 2-fold prolongation of the aPTT. Dipyridamole (0.45 mg/kg/hr for 4 hrs) resulted in a 46 ± 12% and 70 ± 25% reduction of platelet and fibrin accumulation, respectively. Thus, we demonstrated that the dynamics of platelet and fibrin accumulation following balloon injury in rabbits are very different. The vessel wall continues to be thrombogenic for fibrin up to 4 hours after injury even though platelet accumulation has ceased after one hour. We conclude that the local thrombotic events following balloon injury are complex and that not only platelets but also fibrin is important in regulating responses to injury.

Thrombogenicity of the Injured Vessel Wall – Role of Antithrombin and Heparin

1994 ◽  
Vol 71 (01) ◽  
pp. 147-153 ◽  
Author(s):  
Siw Frebelius ◽  
Ulf Hedin ◽  
Jesper Swedenborg
Keyword(s):  
Vessel Wall ◽  
Antithrombin Iii ◽  
Rabbit Aorta ◽  
Continuous Treatment ◽  
Balloon Injury ◽  
Coagulant Activity ◽  
Risk For Thrombosis ◽  
Inhibition Of Thrombin

SummaryThe thrombogenicity of the vessel wall after endothelial denudation is partly explained by an impaired inhibition of thrombin on the subendothelium. We have previously reported that thrombin coagulant activity can be detected on the vessel wall after balloon injury in vivo. The glycosaminoglycans of the subendothelium differ from those of the endothelium and have a lower catalyzing effect on antithrombin III, but inhibition of thrombin can still be augmented by addition of antithrombin III to the injured vessel surface.In this study the effect of antithrombin III and heparin on thrombin coagulant activity on the vessel wall was studied after in vivo balloon injury of the rabbit aorta using biochemical and immunohistochemical methods and thrombin was analysed after excision of the vessel. Continuous treatment with heparin, lasting until sacrifice of the animal, or treatment with antithrombin III resulted in significant reduction of thrombin coagulant activity on the injured aorta. Heparin given only in conjunction with the injury did not prevent thrombin coagulant activity or deposition of fibrin on the surface.The capacity of the injured vessel wall to inhibit thrombin in vitro was improved on aortic segments obtained from animals receiving antithrombin III but not from those given heparin. It is concluded that treatment with antithrombin III interferes with thrombin appearance on the vessel wall after injury and thereby reduces the risk for thrombosis.

Abstract 245: Non-Invasive in vivo Assessment of the Re-Endothelialization Process Using Ultrasound Biomicroscopy in the Rat Carotid Artery Balloon Injury Model

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Samuel Röhl ◽  
Linnea Eriksson ◽  
Robert Saxelin ◽  
Mariette Lengquist ◽  
Kenneth Caidahl ◽  
...  
Keyword(s):  
Carotid Artery ◽  
High Frequency ◽  
Ultrasound Biomicroscopy ◽  
Blue Dye ◽  
High Frequency Ultrasound ◽  
Balloon Injury ◽  
En Face ◽  
In Vivo Assessment ◽  
Frequency Ultrasound

Objective: Ultrasound BioMicroscopy (UBM), or high-frequency ultrasound, is a novel technique used for assessment of anatomy and physiology small research animals. In this study, we evaluate the UBM assessment of the re-endothelialization process following denudation of the carotid artery in rats. Methods: Ultrasound BioMicroscopy data from three different experiments were analyzed. A total of 66 rats of three different strains (Sprague-Dawley, Wistar and Goto-Kakizaki) were included in this study. All animals were subjected to common carotid artery balloon injury and examined with UBM 2 and 4 weeks after injury. Re-endothelialization in UBM was measured as the length from the carotid bifurcation to the distal edge of the intimal hyperplasia. En face staining with Evans-blue dye was performed upon euthanization at 4 weeks after injury followed by tissue harvest for morphological and immunohistochemical evaluation. Results: A significant correlation (Spearman r=0.63,p<0.0001) and an agreement according to Bland-Altman test was identified when comparing all measurements of re-endothelialization in high frequency ultrasound and en face staining. Analysis by animal strain revealed a similar pattern and a significant growth in re-endothelialization length measured in UBM from 2 to 4 weeks could be identified. Immunohistochemical staining for von Willebrand factor confirmed the presence of endothelium in the areas detected as re-endothelialized by the ultrasound assessment. Conclusion: Ultrasound BioMicroscopy can be used for longitudinal in vivo assessment of the re-endothelialization following arterial injury in rats.

Adaptation of Cardinal Points Symmetry Landmarks Distribution Model to in-vivo B-Mode Ultrasound Images of Transverse Cross-section of Carotid Arteries

2021 ◽  
Vol 6 (7) ◽  
pp. 107-113
Author(s):  
Charles Nnamdi Udekwe ◽  
Akinlolu Adediran Ponnle
Keyword(s):  
Carotid Artery ◽  
Cross Section ◽  
Carotid Arteries ◽  
Region Of Interest ◽  
Transverse Cross Section ◽  
Transverse Plane ◽  
Distribution Model ◽  
Ultrasound Images ◽  
Symmetry Line

The geometry of the imaged transverse cross-section of carotid arteries in in-vivo B-mode ultrasound images are most times irregular, unsymmetrical, full of speckles and usually non-uniform. We had earlier developed a technique of cardinal point symmetry landmark distribution model (CPS-LDM) to completely characterize the Region of Interest (ROI) of the geometric shape of thick-walled simulated B-mode ultrasound images of carotid artery imaged in the transverse plane, but this was based on the symmetric property of the image. In this paper, this developed technique was applied to completely characterize the region of interest of the geometric shape of in-vivo B-mode ultrasound images of non-uniform carotid artery imaged in the transverse plane. In order to adapt the CPS-LD Model to the in-vivo carotid artery images, the single VS-VS vertical symmetry line common to the four ROIs of the symmetric image is replaced with each ROI having its own VS-VS vertical symmetry line. This adjustment enables the in-vivo carotid artery images possess symmetric properties, hence, ensuring that all mathematical operations of the CPS-LD Model are conveniently applied to them. This adaptability was observed to work well in segmenting the in-vivo carotid artery images. This paper shows the adaptive ability of the developed CPS-LD Model to successfully annotate and segment in-vivo B-mode ultrasound images of carotid arteries in the transverse cross-sectional plane either they are symmetrical or unsymmetrical.

Local delivery of soluble platelet collagen receptor glycoprotein VI inhibits thrombus formation in vivo

2006 ◽  
Vol 95 (05) ◽  
pp. 763-766 ◽  
Author(s):  
Andreas Bültmann ◽  
Christian Herdeg ◽  
Zhongmin Li ◽  
Götz Münch ◽  
Christine Baumgartner ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Vascular Injury ◽  
Carotid Arteries ◽  
Thrombus Formation ◽  
Critical Role ◽  
Local Delivery ◽  
Computer Assisted ◽  
Glycoprotein Vi ◽  
Collagen Receptor

SummaryPlatelet-mediated thrombus formation at the site of vascular injury isa major trigger for thrombo-ischemic complications after coronary interventions. The platelet collagen receptor glycoprotein VI (GPVI) plays a critical role in the initiation of arterial thrombus formation. Endothelial denudation of the right carotid artery in rabbits was induced through balloon injury. Subsequently, local delivery of soluble, dimeric fusion protein of GPVI (GPVI-Fc) (n=7) or control Fc (n=7) at the site of vascular injury was performed with a modified double-balloon drugdelivery catheter.Thrombus area within the injured carotid artery was quantified using a computer-assisted image analysis and was used as index of thrombus formation.The extent of thrombus formation was significantly reduced in GPVI-Fc- compared with control Fc-treated carotid arteries (relative thrombus area, GPVI-Fc vs. Fc: 9.3 ± 4.2 vs. 2.3 ± 1.7, p<0.001). Local delivery of soluble GPVI resulted in reduced thrombus formation after catheter-induced vascular injury.These data suggest a selective pharmacological modulation of GPVI-collagen interactions to be important for controlling onset and progression of pathological arterial thrombosis, predominantly or even exclusively at sites of injured carotid arteries in the absence of systemic platelet therapy.

scholarly journals Exploring the Relationships Between Hemodynamic Stresses in the Carotid Arteries

2021 ◽  
Vol 7 ◽  
Author(s):  
Magnus Ziegler ◽  
Jesper Alfraeus ◽  
Elin Good ◽  
Jan Engvall ◽  
Ebo de Muinck ◽  
...  
Keyword(s):  
Vessel Wall ◽  
Carotid Arteries ◽  
Carotid Bifurcation ◽  
Vessel Diameter ◽  
Atherosclerotic Plaques ◽  
Shear Stresses ◽  
Strongly Correlated ◽  
4D Flow ◽  
Bifurcation Angle

Background: Atherosclerosis manifests as a focal disease, often affecting areas with complex hemodynamics such as the carotid bifurcation. The magnitude and regularity of the hemodynamic shear stresses acting on the vessel wall are thought to generate risk patterns unique to each patient and play a role in the pathogenesis of atherosclerosis. The involvement of different expressions of shear stress in the pathogenesis of carotid atherosclerosis highlights the need to characterize and compare the differential impact of the various expressions of shear stress in the atherosclerotic carotid bifurcation. Therefore, the aim of this study is to characterize and compare hemodynamic wall shear stresses (WSS) in the carotid arteries of subjects with asymptomatic atherosclerotic plaques. Shear stresses were also compared against vessel diameter and bifurcation angle to examine the relationships with the geometry of the carotid bifurcation.Methods: 4D Flow MRI and contrast-enhanced MRA data were acquired for 245 subjects with atherosclerotic plaques of at least 2.7 mm in conjunction with the Swedish CArdioPulmonary bioImage Study (SCAPIS). Following automatic segmentation and geometric analysis, time-resolved WSS and near-wall turbulent kinetic energy (nwTKE) were derived from the 4D Flow data. Whole-cycle parameters including time-averaged WSS and nwTKE, and the oscillatory shear index (OSI) were calculated. Pairwise Spearman rank-correlation analyses were used to investigate relationships among the hemodynamic as well as geometric parameters.Results: One hundred and seventy nine subjects were successfully segmented using automated tools and subsequently geometric and hemodynamic analyses were performed. Temporally resolved WSS and nwTKE were strongly correlated, ρ = 0.64. Cycle-averaged WSS and nwTKE were moderately correlated, ρ = 0.57. Cycle-average nwTKE was weakly correlated to OSI (ρ = −0.273), revealing that nwTKE provides information about disturbed flow on the vessel wall that OSI does not. In this cohort, there was large inter-individual variation for both WSS and nwTKE. Both WSS and nwTKE varied most within the external carotid artery. WSS, nwTKE, and OSI were weakly correlated to vessel diameter and bifurcation angle.Conclusion: The turbulent and mean component of WSS were examined together in vivo for the first time, and a strong correlation was found between them. nwTKE presents the opportunity to quantify turbulent wall stresses in vivo and gain insight into the effects of disturbed flow on the vessel wall. Neither vessel diameter nor bifurcation angle were found to be strongly correlated to the turbulent or mean component of WSS in this cohort.

Effect Of Selective Inhibition Of Platelet Thromboxane On Platelet-Vessel Wall Interaction In Vivo

1981 ◽  
Author(s):  
Y C Chen ◽  
K K Wu ◽  
E R Hall ◽  
D L Venton ◽  
G C Le Breton
Keyword(s):  
Vessel Wall ◽  
Platelet Reactivity ◽  
Thrombus Formation ◽  
Balloon Catheter ◽  
Specific Inhibitor ◽  
Constant Infusion ◽  
Catheter Technique ◽  
Platelet Thrombus ◽  
Platelet Accumulation

It is well recognized that thromboxane A2(TXA2) plays an important role in platelet reactivity. To determine the role of TXA2 in platelet-vessel wall (P-V) interaction, the effect of 1-benzylimidazole (1-BI), a specific inhibitor of thromboxane synthetase, and 13-azaprostanoic acid (APA), a TXA2 antagonist, on platelet thrombus formation was evaluated in vivo in NZW male rabbits using the autologous indium-111 (111In) labeled platelet technique. Rabbits were treated with intravenous 1-BI or APA or vehicles. After injection of autologous 111In-platelets, de-endothelialization of the abdominal aorta was created by a balloon catheter technique. At 3 hrs, blood samples were obtained and the animals were sacrificed. The aortae were removed and the injured and uninjured segments were dissected. Radioactivity counts and dry weight of the tissues and blood were determined. The vascular radioactivity counts were converted to platelet numbers by using a standard linear calibration curve. As small numbers of platelets adhered to normal vessel wall nonspecifically, this number was subtracted to obtain specific platelet accumulation at the injured sites. 1-BI at 10mg/kg reduced the specific platelet accumulation significantly (n=5, 12.3±S.D.I.5×106 pl/gm tissue; p<0.01) when compared with the controls (n=10, 33.0±5.1×106 pl/gm tissue). Platelet accumulation was further reduced by increasing the dosage to 30mg/kg. By contrast, APA injection (10mg/kg) had no significant effect. However, when APA was given by constant infusion at 250μg/kg/min 1 hr prior to injury, the APA-treated animals had an 80% reduction of platelet accumulation relative to controls. These findings indicate that TXA2 plays an important role in P-V interaction and specific inhibition of TXA2 appears to be efficacious in eliminating platelet thrombus formation.

Evidence for NO involvement in regulating vascular reactivity in balloon-injured rat carotid artery

1995 ◽  
Vol 269 (3) ◽  
pp. H988-H996 ◽  
Author(s):  
T. C. Major ◽  
R. W. Overhiser ◽  
R. L. Panek
Keyword(s):  
Carotid Artery ◽  
Factor Viii ◽  
Vascular Reactivity ◽  
Carotid Arteries ◽  
Muscarinic Agonist ◽  
Ang Ii ◽  
Histomorphometric Analysis ◽  
Balloon Injury ◽  
Contractile Responses ◽  
Endothelin 1

The present study evaluated the influence of this newly formed intima on vascular reactivity in balloon-injured carotid arteries and the regulatory role of the vasodilator, nitric oxide (NO). Balloon injury was performed using a 2-F Fogarty catheter. After 2 and 4 wk, carotid artery segments were removed for both histomorphometric analysis and determination of in vitro contractile responses. Histomorphometric analysis showed a marked intimal thickening with an intima-to-media ratio of 126 +/- 19% (n = 5). The lack of factor VIII staining in injured carotid arteries revealed the absence of endothelium, since factor VIII-related antigen is a glycoprotein synthesized by endothelial cells. Functionally, maximal contractile responses to norepinephrine, angiotensin II (ANG II), endothelin-1, and serotonin were all attenuated in the injured vessels compared with the uninjured carotid arteries [0.38 +/- 0.11 vs. 0.73 +/- 0.10 g (n = 5), norepinephrine; 0.15 +/- 0.06 vs. 0.38 +/- 0.05 g (n = 4), ANG II; 0.60 +/- 0.14 vs. 1.05 +/- 0.12 g (n = 4), endothelin-1; 0.23 +/- 0.07 vs. 0.60 +/- 0.06 g (n = 12), serotonin]. Contractile responses induced by KCl were not affected by the balloon injury (0.62 +/- 0.10 vs. 0.64 +/- 0.09 g, n = 4). Interestingly, carbachol, a muscarinic agonist and vasodilator, caused concentration-dependent relaxations in 2- as well as 4-wk postinjured vessels despite the absence of endothelium. The NO synthase inhibitors, N omega-L-arginine methyl ester (L-NAME) and N omega-nitro-L-arginine (L-NNA), blocked the relaxation responses evoked by carbachol. Exogenously administered L-arginine reversed this blockade of the NOS inhibitors on the carbachol-induced relaxations. In addition, L-NAME partially reversed in a concentration-dependent manner the reduced maximal contractile force elicited by serotonin in the injured carotid artery.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals In vivo cardiovascular magnetic resonance of 2D vessel wall diffusion anisotropy in carotid arteries

2016 ◽  
Vol 18 (1) ◽  
Author(s):  
Peter Opriessnig ◽  
Harald Mangge ◽  
Rudolf Stollberger ◽  
Hannes Deutschmann ◽  
Gernot Reishofer
Keyword(s):  
Cardiovascular Magnetic Resonance ◽  
Magnetic Resonance ◽  
Vessel Wall ◽  
Carotid Arteries ◽  
Diffusion Anisotropy

scholarly journals Quantitative susceptibility mapping improves the detection of calcified carotid vessels by multi-contrast MRI using computed tomography angiography as the reference standard

2021 ◽  
Author(s):  
Thanh D Nguyen ◽  
Yan Wen ◽  
Jingwen Du ◽  
Pascal Spincemaille ◽  
Yi Wang ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Carotid Artery ◽  
Vessel Wall ◽  
Carotid Arteries ◽  
Susceptibility Mapping ◽  
Reference Standard ◽  
Quantitative Susceptibility Mapping ◽  
Vessel Detection ◽  
Carotid Vessel Wall ◽  
Carotid Vessels

The objective of this study was to evaluate initial feasibility and improvement in the detection of calcified carotid arteries by including quantitative susceptibility mapping (QSM) in the carotid vessel wall multi-contrast MRI (mcMRI) protocol using CTA as the reference standard. In a pilot cohort of ten patients with significant carotid artery stenosis, calcified vessel detection by mcMRI achieved 64.7% sensitivity and 100% specificity. Adding QSM to mcMRI improved sensitivity to 100% while not affecting specificity.

Direct Real Time Visualization of Platelet Calclium Signaling In Vivo: Role of Platelet Activation and Thrombus Formation in a Living Mouse.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 325-325 ◽  
Author(s):  
Christophe Dubois ◽  
Laurence Panicot-Dubois ◽  
Barbara C. Furie ◽  
Bruce Furie
Keyword(s):  
Intracellular Calcium ◽  
Platelet Activation ◽  
Vessel Wall ◽  
High Speed ◽  
Critical Role ◽  
Calcium Mobilization ◽  
Recipient Mouse ◽  
Intracellular Calcium Mobilization ◽  
Platelet Accumulation

Abstract Intracellular calcium mobilization plays a critical role in platelet signaling. Upon platelet activation, an intracellular calcium mobilization leads to the activation of various intracellular and membrane proteins, including integrins involved in both platelet shape change and aggregation. The goal of the present study was to monitor platelet calcium mobilization in vivo in an intact animal and to determine which intracellular pathways are dominant in platelet accumulation into the developing thrombus. Platelets were isolated from mice, washed, loaded with a calcium-sensitive fluorochrome, Fura2-AM and then infused into a recipient mouse. We studied Fura2-AM loaded platelet incorporation during arterial thrombus development following laser injury of the vessel wall in the cremaster microcirculation of living mice using high speed intravital widefield digital microscopy. Fura-2 loaded platelets were monitored by excitation at 380 nm; this fluorescence reports the basal calcium levels in platelets. Calcium mobilization was monitored by excitation at 340 nm where the fluorescence intensity reflects Fura2-calcium complex formation. We observed that platelets bind to the growing thrombus independent of calcium mobilization. However, the stable incorporation of platelets into the thrombus correlated with a significant intracellular calcium increase. Once the thrombus reached maximal size at about 100 seconds, the calcium mobilization also reached maximal intensity. Subsequently, platelets that did not mobilize calcium dissociated from the thrombus. We confirmed these observations by using platelets treated with the calcium chelators, BAPTA-AM or EGTA-AM. We observed a significant inhibition of platelet accumulation into the thrombus, indicating that the intracellular calcium increase is necessary in vivo for the stable accumulation of the platelets into the thrombus. We also evaluated the involvement in vivo of two platelet agonists, ADP and thromboxane A2 (TxA2), on calcium mobilization and platelet incorporation into thrombi. When platelets were treated with aspirin or with the P2Y1 antagonist A3P5P (adenosine 3′-phosphate-5′-phosphate), we observed a partial decrease in both calcium mobilization and platelet accumulation into the thrombus. These results indicate that TxA2 and ADP via the P2Y1 receptor are involved in vivo in platelet activation upon vessel wall injury in this thrombosis model. When platelets were treated with both compounds, we completely inhibited the calcium increase and the incorporation of platelets into the thrombus. Altogether, our results directly show, for the first time in vivo, the importance of the calcium mobilization on platelet accumulation into the developing thrombus. The platelet agonists TxA2 and ADP both play an important and complementary role on platelet activation by acting on the mobilization of the intracellular calcium.

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