Pravastatin reduces myocardial lesions induced by acute inhibition of nitric oxide biosynthesis in normocholesterolemic rats

dc.creatorCoelho, OR
dc.creatorDe Luca, IMS
dc.creatorTanus-Santos, JE
dc.creatorCittadino, M
dc.creatorSampaio, RC
dc.creatorCoelho, OR
dc.creatorHyslop, S
dc.creatorMoreno, H
dc.date2001
dc.dateJUL
dc.date2014-11-14T23:49:43Z
dc.date2015-11-26T16:08:53Z
dc.date2014-11-14T23:49:43Z
dc.date2015-11-26T16:08:53Z
dc.date.accessioned2018-03-28T22:57:28Z
dc.date.available2018-03-28T22:57:28Z
dc.identifierInternational Journal Of Cardiology. Elsevier Sci Ireland Ltd, v. 79, n. 41700, n. 215, n. 221, 2001.
dc.identifier0167-5273
dc.identifierWOS:000170267100019
dc.identifier10.1016/S0167-5273(01)00423-5
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/81178
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/81178
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/81178
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1266477
dc.descriptionPravastatin is useful in restoring endothelium-dependent relaxation in hypercholesterolemic animals. A single intravenous bolus injection of N-omega-nitro-L-arginine methyl ester (L-NAME), a non-specific inhibitor of NO synthase, causes myocardial necrosis and reduces coronary flow in rats. Since rats do not develop hypercholesterolemia and atherosclerosis, we have tested the hypothesis that pravastatin protects the heart from myocardial lesions induced by L-NAME in the absence of alterations in cholesterol levels and plaque formation. Male Wistar rats fed standard chow were divided into four groups: CONTROL (n=14) - rats that received tap water alone for 18 days; L-NAME (n=14) - rats that received L-NAME (15 mg/kg, i.v.) on the 14th day of the study; PRAVASTATIN (n=11) - rats that received pravastatin (6 mg/kg/day) in their drinking water for 18 days; PRAVASTATIN+L-NAME (n=12) - rats that received pravastatin (6 mg/kg/day) and L-NAME (15 mg/kg, i.v.) as indicated in the preceding groups. At the end of 18 days, the rats were sacrificed and the hearts removed for stereological analysis by light microscopy. Plasma nitrate/nitrite and thromboxane B-2 concentrations were determined immediately before and after L-NAME administration. Pravastatin prevented the ischemic lesions induced by the acute inhibition of NO biosynthesis (the area of myocardial lesions in the L-NAME group was greater than in the Pravastatin+L-NAME group: 101.6 mum(2) vs. 1.2 mum(2), respectively; P <0.0001) and markedly increased the plasma nitrate/nitrate concentrations, even before L-NAME administration. There were no significant changes in the plasma thromboxane B-2 concentrations. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.
dc.description79
dc.description41700
dc.description215
dc.description221
dc.languageen
dc.publisherElsevier Sci Ireland Ltd
dc.publisherClare
dc.publisherIrlanda
dc.relationInternational Journal Of Cardiology
dc.relationInt. J. Cardiol.
dc.rightsfechado
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.sourceWeb of Science
dc.subjectHMG-CoA reductase inhibitors
dc.subjectpravastatin
dc.subjectendothelium
dc.subjectL-NAME
dc.subjectthromboxane
dc.subjectmyocardial infarction
dc.subjecthypertension
dc.subjectCoa Reductase Inhibitors
dc.subjectHypercholesterolemic Rabbits
dc.subjectSimvastatin
dc.subjectCholesterol
dc.subjectSynthase
dc.subjectStatins
dc.subjectLipoproteins
dc.subjectFluvastatin
dc.subjectIschemia
dc.subjectProtein
dc.titlePravastatin reduces myocardial lesions induced by acute inhibition of nitric oxide biosynthesis in normocholesterolemic rats
dc.typeArtículos de revistas


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