Local Delivery of Heparin Into Rabbit Carotid Artery With a Novel Electroporation Catheter

Endothelium-dependent relaxations to acetylcholine remain normal in the carotid artery of hypercholesterolemic rabbits, but unlike endothelium-dependent relaxations of normal rabbits, they are inhibited by charybdotoxin, a specific blocker of Ca(2+)-dependent K+ channels. Because nitric oxide (NO) is the mediator of endothelium-dependent relaxation and can activate Ca(2+)-dependent K+ channels directly or via guanosine 3',5'-cyclic monophosphate, the present study investigated the role of Ca(2+)-dependent K+ channels in relaxations caused by NO, sodium nitroprusside, and 8-bromoguanosine 3',5'-cyclic monophosphate (8-Brc-GMP) in hypercholesterolemic rabbit carotid artery. Isometric tension was measured in rabbit carotid artery denuded of endothelium from normal and hypercholesterolemic rabbits which were fed 0.5% cholesterol for 12 wk. Under control conditions, relaxations to all agents were similar in normal and hypercholesterolemic rabbit arteries. Charybdotoxin had no significant effect on relaxations of normal arteries to NO, sodium nitroprusside, or 8-BrcGMP, but the Ca(2+)-dependent K+ channel blocker significantly inhibited the relaxations caused by each of these agents in the arteries from hypercholesterolemic rabbits. By contrast, relaxations to the calcium channel blocker nifedipine were potentiated to a similar extent by charybdotoxin in both groups. In addition, arteries from hypercholesterolemic rabbits relaxed less than normal to sodium nitroprusside when contracted with depolarizing potassium solution. These results indicate that although nitrovasodilator relaxations are normal in the hypercholesterolemic rabbit carotid artery, they are mediated differently, and to a greater extent, by Ca(2+)-dependent K+ channels. These data also suggest that K+ channel-independent mechanism(s) are impaired in hypercholesterolemia.

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199. Circulating Endothelial Progenitor Cells Restore Endothelial Function of Balloon Injured Rabbit Carotid Artery

Molecular Therapy ◽

10.1016/j.ymthe.2004.06.107 ◽

2004 ◽

Vol 9 ◽

pp. S77

Keyword(s):

Carotid Artery ◽

Endothelial Function ◽

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Endothelial Progenitor ◽

Rabbit Carotid Artery ◽

Circulating Endothelial Progenitor Cells

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The Antiaggregating and Antithrombotic Activity of Clopidogrel Is Potentiated by Aspirin in Several Experimental Models in the Rabbit

Thrombosis and Haemostasis ◽

10.1055/s-0037-1615238 ◽

1998 ◽

Vol 80 (09) ◽

pp. 512-518 ◽

Cited By ~ 75

Author(s):

Frédérique Dol ◽

André Bernat ◽

Robert Falotico ◽

Alain Lalé ◽

Pierre Savi ◽

...

Keyword(s):

Platelet Aggregation ◽

Carotid Artery ◽

Ex Vivo ◽

Thrombus Formation ◽

Experimental Models ◽

Arteriovenous Shunt ◽

Thrombotic Occlusion ◽

Antithrombotic Activity ◽

Rabbit Carotid Artery ◽

Antithrombotic Efficacy

SummaryIt is unknown whether the addition of aspirin might increase both the efficacy and the potency of clopidogrel, a potent and selective ADP blocker. For that purpose, the efficacy of clopidogrel (1–20 mg/kg, p.o.) administered orally to rabbits alone or in combination with aspirin (0.1–10 mg/kg, p.o.) was determined in several experimental models. A potent synergistic effect of the clopidogrel/aspirin association was demonstrated with regard to collagen-induced platelet aggregation measured ex vivo. Similarly, aspirin potentiated the antithrombotic activity of clopidogrel measured with regard to experimental thrombosis induced by a silk thread or on stents placed in an arteriovenous shunt, thrombus formation following electrical stimulation of the rabbit carotid artery and with regard to 111In-labeled platelet deposition on a stent implanted in an arteriovenous shunt or on the subendothelium following air drying injury of the rabbit carotid artery. A similar potentiating effect of aspirin was obtained with regard to myointimal proliferation (restenosis) in the femoral arteries of atherosclerotic rabbits which occurred as a consequence of stent placement. The clopidogrel/aspirin combination showed only additive-type effects on bleeding time prolongation induced by ear transection in the rabbit, therefore showing that combined inhibition of cyclooxygenase and ADP‘s effects provide a marked enhanced antithrombotic efficacy. Such a combination may provide substantial protection against platelet aggregation leading to thrombotic occlusion at sites of endothelial injuries and coronary artery stenosis in humans.

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

Thrombosis and Haemostasis ◽

10.1160/th05-11-0731 ◽

2006 ◽

Vol 95 (05) ◽

pp. 763-766 ◽

Cited By ~ 31

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.

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The Effect of Smooth Muscle Activity on the Static and Dynamic Elastic Properties of the Rabbit Carotid Artery

Cardiovascular System Dynamics ◽

10.1007/978-1-4899-6693-3_39 ◽

1982 ◽

pp. 393-402 ◽

Cited By ~ 2

Author(s):

D. L. Newman ◽

S. E. Greenwald

Keyword(s):

Smooth Muscle ◽

Carotid Artery ◽

Elastic Properties ◽

Muscle Activity ◽

Rabbit Carotid Artery ◽

Dynamic Elastic Properties

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Investigation of changes in vWF expression in rabbit carotid artery collar model

Journal of Dr Behcet Uz Children s Hospital ◽

10.5222/buchd.2018.037 ◽

2018 ◽

Author(s):

Mehmet Zuhuri Arun ◽

Gülnur Sevin ◽

Günay Yetik Anacak ◽

Ceren Gönen Korkmaz ◽

Levent Üstünes

Keyword(s):

Carotid Artery ◽

Rabbit Carotid Artery

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Endothelium-dependent hyperpolarization elicited by adenine compounds in rabbit carotid artery

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1991.260.4.h1037 ◽

1991 ◽

Vol 260 (4) ◽

pp. H1037-H1042 ◽

Cited By ~ 1

Author(s):

G. Chen ◽

H. Suzuki

Keyword(s):

Smooth Muscle ◽

Carotid Artery ◽

Direct Action ◽

Smooth Muscles ◽

Muscle Membrane ◽

Dependent Manner ◽

Rabbit Carotid Artery ◽

Mechanical Removal ◽

Smooth Muscle Membrane ◽

Adventitial Cells

Electrical responses of the membrane of intimal and adventitial smooth muscle cells of the rabbit carotid artery to ATP, ADP, AMP, and adenosine were recorded. In intimal cells, these compounds hyperpolarized the membrane. Mechanical removal of the endothelium altered the responses to ATP and ADP to one of a transient depolarization, with no alteration of the response to AMP and adenosine. In the adventitial cells, ATP and ADP produced a transient depolarization, whereas AMP and adenosine produced a sustained hyperpolarization, irrespective of the presence or absence of the endothelium. In tissues with an intact endothelium, 5'-adenylylimidodiphosphate tetralithium salt and alpha,beta-methylene ATP (mATP) transiently depolarized the membrane in these smooth muscles. In case of stabilization with mATP, only hyperpolarization was generated by ATP, in an endothelium-dependent manner. Our interpretation of these observations is that 1) ATP and ADP depolarize smooth muscle membrane by a direct action and hyperpolarize the membrane indirectly through the release of endothelium-derived hyperpolarizing factor, 2) AMP and adenosine hyperpolarize the membrane, independently of the endothelium, and 3) ATP receptors present on the endothelial cell membrane differ from those on smooth muscle membrane.

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