| Balloon catheter injury abolishes phenylephrine-induced relaxation in the rat contralateral carotid. | |
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MedLine Citation:
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PMID: 21323906 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND AND PURPOSE: The consequences of compensatory responses to balloon catheter injury in rat carotid artery, on phenylephrine-induced relaxation and contraction in the contralateral carotid artery were studied. EXPERIMENTAL APPROACH: Relaxation and contraction concentration-response curves for phenylephrine were obtained for contralateral carotid arteries in the presence of indomethacin (COX inhibitor), SC560 (COX-1 inhibitor), SC236 (COX-2 inhibitor) or 4-hydroxytetramethyl-L-piperidine-1-oxyl (tempol; superoxide dismutase mimetic). Reactive oxygen species were measured in carotid artery endothelial cells fluorimetrically with dihydroethidium. KEY RESULTS: Phenylephrine-induced relaxation was abolished in contralateral carotid arteries from operated rats (E(max) = 0.01 ± 0.004 g) in relation to control (E(max) = 0.18 ± 0.005 g). Phenylephrine-induced contractions were increased in contralateral arteries (E(max) = 0.54 ± 0.009 g) in relation to control (E(max) = 0.38 ± 0.014 g). SC236 restored phenylephrine-induced relaxation (E(max) = 0.17 ± 0.004 g) and contraction (E(max) = 0.34 ± 0.018 g) in contralateral arteries. Tempol restored phenylephrine-induced relaxation (E(max) = 0.19 ± 0.012 g) and contraction (E(max) = 0.42 ± 0.014 g) in contralateral arteries, while apocynin did not alter either relaxation (E(max) = 0.01 ± 0.004 g) or contraction (E(max) = 0.54 ± 0.009 g). Dihydroethidium fluorescence was increased in contralateral samples (18 882 ± 435 U) in relation to control (10 455 ± 303 U). SC236 reduced the fluorescence in contralateral samples (8250 ± 365 U). CONCLUSIONS AND IMPLICATIONS: Balloon catheter injury abolished phenylephrine-induced relaxation and increased phenylephrine-induced contraction in contralateral carotid arteries, through O(2) (-) derived from COX-2. |
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Authors:
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L Pernomian; Ms Gomes; Am de Oliveira |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: British journal of pharmacology Volume: 163 ISSN: 1476-5381 ISO Abbreviation: Br. J. Pharmacol. Publication Date: 2011 Jun |
Date Detail:
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Created Date: 2011-05-27 Completed Date: 2011-10-06 Revised Date: 2012-09-19 |
Medline Journal Info:
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Nlm Unique ID: 7502536 Medline TA: Br J Pharmacol Country: England |
Other Details:
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Languages: eng Pagination: 770-81 Citation Subset: IM |
Copyright Information:
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© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society. |
Affiliation:
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Department of Pharmacology, School of Medicine of Ribeirão Preto, Laboratory of Pharmacology, University of São Paulo, Brazil. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Angioplasty, Balloon, Coronary
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adverse effects* Animals Carotid Arteries / drug effects*, metabolism, physiology Carotid Artery Injuries / metabolism, physiopathology* Cyclic N-Oxides / pharmacology Cyclooxygenase Inhibitors / pharmacology Endothelium, Vascular / drug effects, injuries Indomethacin / pharmacology Male Muscle Contraction / drug effects* Muscle, Smooth, Vascular / drug effects, metabolism NADP / metabolism NADPH Oxidase / metabolism Oxygen / metabolism Phenylephrine / pharmacology* Prostaglandin-Endoperoxide Synthases / metabolism Pyrazoles / pharmacology Rats Rats, Wistar Reactive Oxygen Species / metabolism Spin Labels Sulfonamides / pharmacology Vasodilation / drug effects* |
| Chemical | |
Reg. No./Substance:
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0/4-(5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide; 0/Cyclic N-Oxides; 0/Cyclooxygenase Inhibitors; 0/Pyrazoles; 0/Reactive Oxygen Species; 0/SC 560; 0/Spin Labels; 0/Sulfonamides; 2226-96-2/tempol; 53-59-8/NADP; 53-86-1/Indomethacin; 59-42-7/Phenylephrine; 7782-44-7/Oxygen; EC 1.14.99.1/Prostaglandin-Endoperoxide Synthases; EC 1.6.3.1/NADPH Oxidase |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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