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    Carvedilol inhibits aortic lipid deposition in the hypercholesterolemic rat

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    Authors
    Feuerstein, Giora Z.
    Fisher, Marc
    Nunnari, John J.
    Ruffolo, Robert R. Jr.
    UMass Chan Affiliations
    Department of Neurology
    Document Type
    Journal Article
    Publication Date
    1997-01-01
    Keywords
    Adrenergic beta-Antagonists
    Animals
    Aorta, Thoracic
    Arteriosclerosis
    Calcium Channel Blockers
    Carbazoles
    Hypercholesterolemia
    *Lipid Metabolism
    Male
    Nifedipine
    Propanolamines
    Rats
    Rats, Wistar
    Vasodilator Agents
    Nervous System Diseases
    Neurology
    Pharmacy and Pharmaceutical Sciences
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    Link to Full Text
    http://www.karger.com/Article/Pdf/139466
    Abstract
    The effects of carvedilol, a vasodilating beta-blocker with antioxidant activity, and nifedipine, a calcium channel blocker, were investigated on aortic lipid deposition and the accumulation of monocytes and foam cells at the sites of atherosclerotic lesions in rats subjected to a hypercholesterolemic diet. Fifty rats were randomly assigned to the following experimental groups: (1) regular rat chow (n = 5); (2) regular rat chow supplemented with a high-cholesterol diet (1% cholesterol and 1% cholic acid; n = 15); (3) a high-cholesterol diet plus nifedipine (n = 15), and (4) a high-cholesterol diet plus carvedilol (n = 15). Animals were maintained on these diets for 12 weeks. None of the treatment groups had blood pressures that were outside the normotensive range, and no significant differences in plasma lipid levels were observed among the high-cholesterol diet and drug-treated groups. There was a significantly lower lipid content (p < 0.001) in the thoracic aortas of the nifedipine-treated (211 +/- 23 nmol/mm2) and carvedilol-treated (182 +/- 23 nmol/mm2) groups compared to cholesterol-fed controls (242 +/- 27 nmol/mm2). Furthermore, carvedilol-treated animals showed significantly less (p < 0.001) lipid accumulation than did the nifedipine-treated animals. The number of monocytes and foam cells were decreased in both drug-treated groups compared to animals receiving high-cholesterol diets without drug treatment. The results demonstrate that treatment with carvedilol or nifedipine can significantly inhibit lipid deposition in the aorta and reduce monocyte and foam cell accumulation, and that carvedilol is significantly more effective than nifedipine in inhibiting lipid deposition.
    Source
    Pharmacology. 1997 Jan;54(1):24-32.
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/37817
    PubMed ID
    9065958
    Related Resources
    Link to article in PubMed
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    UMass Chan Faculty and Researcher Publications

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