dc.creatorJorge, PAR
dc.creatorOsaki, MR
dc.creatorDeAlmeida, E
dc.creatorDalva, M
dc.creatorNeto, LC
dc.date1997
dc.dateFEB
dc.date2014-12-16T11:37:14Z
dc.date2015-11-26T17:27:37Z
dc.date2014-12-16T11:37:14Z
dc.date2015-11-26T17:27:37Z
dc.date.accessioned2018-03-29T00:14:45Z
dc.date.available2018-03-29T00:14:45Z
dc.identifierExperimental And Toxicologic Pathology. Gustav Fischer Verlag, v. 49, n. 41671, n. 147, n. 151, 1997.
dc.identifier0940-2993
dc.identifierWOS:A1997WP78900023
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/64777
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/64777
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/64777
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1284842
dc.descriptionThe aim of the present report was to study the effect of ischemia-reperfusion on the endothelial cell function of coronary vessels. Twelve adult male dogs were instrumented for the measurement of aortic and left ventricular pressures, heart rate and coronary blood flow. The left anterior descending coronary artery was occluded for 90 minutes followed by 20 minutes of reperfusion. Acetylcholine was infused into the coronary artery at a rate of 15 mu g/kg/min. Coronary flow, heart rate and aortic and left ventricular pressures were registered during the pre-occlusion period and after 20 minutes of reperfusion under basal conditions, as well as during acetylcholine administration. These same parameters were also measured during reactive hyperemia following vessel deocclusion. Acetylcholine produced a 155 % increasing coronary flow during the pre-occlusion period (p < 0.05). In the reperfusion period, no statistically significant difference was observed between the flows in the presence and absence of this substance, nor were there any differences in the other cardiovascular parameters monitored. Triphenyltetrazolium staining confirmed myocardial infarction in all the hearts examined. The authors conclude that reperfusion following myocardial infarction prevents the increasing in coronary flow in response to acetylcholine as a result of endothelial dysfunction in the resistance coronary vessels.
dc.description49
dc.description41671
dc.description147
dc.description151
dc.languageen
dc.publisherGustav Fischer Verlag
dc.publisherJena
dc.publisherAlemanha
dc.relationExperimental And Toxicologic Pathology
dc.relationExp. Toxicol. Pathol.
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectblood flow, coronary
dc.subjectcoronary blood flow
dc.subjectendothelium, coronary
dc.subjectischemia, heart
dc.subjectheart, ischemia
dc.subjectcardiac ischemia reperfusion, coronary
dc.subjectacetylcholine
dc.subjectMyocardial Infarct Size
dc.subjectBlood-flow
dc.subjectSuperoxide-dismutase
dc.subjectNo-reflow
dc.subjectInjury
dc.subjectReactivity
dc.subjectOcclusion
dc.subjectDogs
dc.subjectQuantification
dc.subjectDysfunction
dc.titleEndothelium-dependent coronary flow in ischemia reperfusion
dc.typeArtículos de revistas


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