scholarly journals AB063. 82. Development of a porcine urethral model to characterize the effect of catheter balloon injury on the paediatric urethra

2019 ◽  
Vol 3 ◽  
pp. AB063-AB063
Author(s):  
Stefanie Croghan ◽  
Rachel Cahalane ◽  
Ivan Cassidy ◽  
Niall Davis ◽  
Rory Mooney ◽  
...  
Keyword(s):  
Balloon Injury ◽  
Urethral Model

Radiolabeled r-Hirudin as a Measure of Thrombin Activity at, or within, the Rabbit Aorta Wall In Vitro and In Vivo

1994 ◽  
Vol 71 (04) ◽  
pp. 499-506 ◽  
Author(s):  
Mark W C Hatton ◽  
Bonnie Ross-Ouellet
Keyword(s):  
Rabbit Aorta ◽  
Balloon Injury ◽  
Recombinant Hirudin ◽  
Aorta Wall ◽  
Thrombin Activity ◽  
Before And After ◽  
The Matrix

SummaryThe behavior of 125I-labeled recombinant hirudin towards the uninjured and de-endothelialized rabbit aorta wall has been studied in vitro and in vivo to determine its usefulness as an indicator of thrombin activity associated with the aorta wall. Thrombin adsorbed to either sulfopropyl-Sephadex or heparin-Sepharose bound >95% of 125I-r-hirudin and the complex remained bound to the matrix. Binding of 125I-r-hirudin to the exposed aorta subendothelium (intima-media) in vitro was increased substantially if the tissue was pre-treated with thrombin; the quantity of l25I-r-hirudin bound to the de-endothelialized intima-media (i.e. balloon-injured in vitro) correlated positively with the quantity of bound 131I-thrombin (p <0.01). Aortas balloon-injured in vivo were measured for thrombin release from, and binding of 125I-r-hirudin to, the de-endothelialized intimal surface in vitro; 125I-r-hirudin binding correlated with the amount of active thrombin released (p <0.001). Uptake of 125I-r-hirudin by the aorta wall in vivo was proportional to the uptake of 131I-fibrinogen (as an indicator of thrombin activity) before and after balloon injury. After 30 min in the circulation, specific 125I-r-hirudin binding to the uninjured and de-endo- thelialized (at 1.5 h after injury) aorta wall was equivalent to 3.4 (± 2.5) and 25.6 (±18.1) fmol of thrombin/cm2 of intima-media, respectively. Possibly, only hirudin-accessible, glycosaminoglycan-bound thrombin is measured in this way.

Targeting Platelets Containing Electro-encapsulated lloprost to Balloon Injured Aorta in Rats

1995 ◽  
Vol 73 (03) ◽  
pp. 535-542 ◽  
Author(s):  
N Crawford ◽  
A Chajara ◽  
G Pfliegler ◽  
B EI Gamal ◽  
L Brewer ◽  
...  
Keyword(s):  
Time Course ◽  
Therapeutic Potential ◽  
Simple Procedure ◽  
Rat Aorta ◽  
Balloon Injury ◽  
Post Injury ◽  
Antiproliferative Effects ◽  
Platelet Deposition ◽  
Total Dna ◽  
Novel Drug

SummaryDrugs can be electro-encapsulated within platelets and targeted to damaged blood vessels by exploiting the platelet’s natural haemostatic properties to adhere to collagen and other vessel wall constituents revealed by injury. A rat aorta balloon angioplasty model has been used to study the effect on platelet deposition of giving iloprost loaded platelets i.v. during the balloon injury. After labelling the circulating platelets with 111-Indium before balloon injury, time course studies showed maximum platelet deposition on the injured aorta occurred at about 1 h post-injury and the deposition remained stable over the next 2-3 h. When iloprost-loaded platelets were given i.v. during injury and the circulating platelet pool labelled with 111-Indium 30 min later, platelet deposition, measured at 2 h postinjury, was substantially and significantly reduced compared with control platelet treatment. Some antiproliferative effects of iloprost-loaded platelets given i.v. during injury have also been observed. Whereas the incorporation of [3H]-thymidine into aorta intima-media DNA at 3 days post injury was 62-fold higher in balloon injured rats than in control sham operated rats, thymidine incorporation into intima/media of rats which had received iloprost loaded platelets during injury was reduced as compared with rats subjected only to the injury procedure. The reduction was only of near significance, however, but at 14 days after injury the total DNA content of the aorta intima/media of rats given iloprost loaded platelets during injury was significantly reduced. Although iloprost loaded platelets can clearly inhibit excessive platelet deposition, other encapsulated agents may have greater anti-proliferative effects. These studies have shown that drug loaded platelets can be targeted to injured arteries, where they may be retained as depots for local release. We believe this novel drug delivery protocol may have therapeutic potential in reducing the incidence of occlusion and restenosis after angioplasty and thrombolysis treatment. Electro-encapsulation of drugs into platelets is a simple procedure and, using autologous and fully biocompatible and biodegradable platelets as delivery vehicles, might overcome some of the immunological and toxicological problems which have been encountered with other delivery vectors such as liposomes, microbeads, synthetic microcapsules and antibodies.

Smooth Muscle DNA Replication in Response to Angiotensin II Is Regulated Differently in the Neointima and Media at Different Times After Balloon Injury in the Rat Carotid Artery

1996 ◽  
Vol 16 (9) ◽  
pp. 1130-1137 ◽  
Author(s):  
D. deBlois ◽  
M. Viswanathan ◽  
J.E. Su ◽  
A.W. Clowes ◽  
J.M. Saavedra ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Dna Replication ◽  
Angiotensin Ii ◽  
Carotid Artery ◽  
Balloon Injury

Medroxyprogesterone Attenuates Estrogen-Mediated Inhibition of Neointima Formation After Balloon Injury of the Rat Carotid Artery

Circulation ◽  
1996 ◽  
Vol 94 (9) ◽  
pp. 2221-2227 ◽  
Author(s):  
Ronald L. Levine ◽  
Shi-Juan Chen ◽  
Joan Durand ◽  
Yiu-Fai Chen ◽  
Suzanne Oparil
Keyword(s):  
Carotid Artery ◽  
Neointima Formation ◽  
Balloon Injury

Basic Fibroblast Growth Factor Restores Endothelium-Dependent Responses After Balloon Injury of Rabbit Arteries

Circulation ◽  
1996 ◽  
Vol 93 (1) ◽  
pp. 18-22 ◽  
Author(s):  
Thibaud Meurice ◽  
Christophe Bauters ◽  
Jean-Luc Auffray ◽  
Benoı̂t Vallet ◽  
Martial Hamon ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Fibroblast Growth ◽  
Balloon Injury

Induction of Renin in Medial Smooth Muscle Cells by Balloon Injury

Hypertension ◽  
1997 ◽  
Vol 29 (4) ◽  
pp. 1044-1050 ◽  
Author(s):  
Naoharu Iwai ◽  
Masafumi Izumi ◽  
Tadashi Inagami ◽  
Masahiko Kinoshita
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Balloon Injury

scholarly journals The effect of 17 β estradiol on the severe atherosclerosis induced by high cholesterol diet plus balloon injury through the NO

1997 ◽  
Vol 75 ◽  
pp. 54
Author(s):  
E. Muto ◽  
T. Hayashi ◽  
T. Esaki ◽  
H. Kano ◽  
N.K. Thakur ◽  
...  
Keyword(s):  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Balloon Injury ◽  
Severe Atherosclerosis

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.

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