On the oxygen consumption of intact vessel wall segments and intima-media preparations of the rabbit carotid artery

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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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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Microvascular oxygen delivery and consumption following treatment with verapamil

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00955.2004 ◽

2005 ◽

Vol 288 (4) ◽

pp. H1515-H1520 ◽

Cited By ~ 13

Author(s):

Nanae Hangai-Hoger ◽

Amy G. Tsai ◽

Barbara Friesenecker ◽

Pedro Cabrales ◽

Marcos Intaglietta

Keyword(s):

Oxygen Consumption ◽

Vessel Wall ◽

Muscle Relaxation ◽

Capillary Density ◽

Smooth Muscle Relaxation ◽

Oxygen Release ◽

Total Oxygen ◽

Verapamil Hcl ◽

Window Chamber ◽

Vascular Smooth Muscle Relaxation

The microvascular distribution of oxygen was studied in the arterioles and venules of the awake hamster window chamber preparation to determine the contribution of vascular smooth muscle relaxation to oxygen consumption of the microvascular wall during verapamil-induced vasodilatation. Verapamil HCl delivered in a 0.1 mg/kg bolus injection followed by a continuous infusion of 0.01 mg·kg−1·min−1 caused significant arteriolar dilatation, increased microvascular flow and functional capillary density, and decreased arteriolar vessel wall transmural Po2 difference. Verapamil caused tissue Po2 to increase from 25.5 ± 4.1 mmHg under control condition to 32.0 ± 3.7 mmHg during verapamil treatment. Total oxygen released by the microcirculation to the tissue remained the same as at baseline. Maintenance of the same level of oxygen release to the tissue, increased tissue Po2, and decreased wall oxygen concentration gradient are compatible if vasodilatation significantly lowers vessel wall oxygen consumption, which in this model appears to constitute an important oxygen-consuming compartment. These findings show that treatment with verapamil, which increases oxygen supply through vasodilatation, may further improve tissue oxygenation by lowering oxygen consumption of the microcirculation.

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