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Article: Acute impairment of endothelium-dependent relaxations to aggregating platelets following reperfusion injury in canine coronary arteries

TitleAcute impairment of endothelium-dependent relaxations to aggregating platelets following reperfusion injury in canine coronary arteries
Authors
Issue Date1990
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org
Citation
Circulation Research, 1990, v. 67 n. 2, p. 385-393 How to Cite?
AbstractExperiments were designed to determine whether endothelial injury contributes to augmented coronary vascular tone seen during myocardial reperfusion. Canine left anterior descending coronary arteries were exposed to ischemia followed by reperfusion (60 minutes each). Rings (3-4 mm) of the reperfused artery and of normal left circumflex (control) coronary artery segments were prepared. Rings were suspended for isometric force measurement in organ chamber containing modified Krebs' Ringer bicarbonate solution (37°C, 95%, O2-5% CO2). Endothelium-independent contractions to KCl and prostaglandin F(2α) were unaltered after reperfusion. Endothelium-dependent relaxations to nitric oxide, sodium nitroprusside, and isoproterenol were comparable in control and reperfused arteries. However, reperfused coronary arteries contracted with prostaglandin F(2α) lost the ability to express endothelium-dependent relaxations to aggregating platelets. Reperfused arterial rings also exhibited impaired endothelium-dependent relaxations to acetylcholine, the calcium ionophore A23187, and the platelet-derived compounds ADP and serotonin. Quiescent (noncontracted) reperfused arterial rings exhibited larger conractions than controls when exposed to aggregating platelets. In such quiescent rings, the endothelium-dependent increase in tension to hemoglobin was unaltered after reperfusion. Thus, coronary reperfusion impairs the normal endothelium-dependent relaxations to aggregating platelets and vasoactive drugs. This impairment of platelet-mediated coronary relaxtion could help explain the increased vascular tone and tendency toward vasospasm commonly observed after reperfusion of the coronary arteries.
Persistent Identifierhttp://hdl.handle.net/10722/170995
ISSN
2015 Impact Factor: 11.551
2015 SCImago Journal Rankings: 5.755
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorPearson, PJen_US
dc.contributor.authorSchaff, HVen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:45Z-
dc.date.available2012-10-30T06:11:45Z-
dc.date.issued1990en_US
dc.identifier.citationCirculation Research, 1990, v. 67 n. 2, p. 385-393en_US
dc.identifier.issn0009-7330en_US
dc.identifier.urihttp://hdl.handle.net/10722/170995-
dc.description.abstractExperiments were designed to determine whether endothelial injury contributes to augmented coronary vascular tone seen during myocardial reperfusion. Canine left anterior descending coronary arteries were exposed to ischemia followed by reperfusion (60 minutes each). Rings (3-4 mm) of the reperfused artery and of normal left circumflex (control) coronary artery segments were prepared. Rings were suspended for isometric force measurement in organ chamber containing modified Krebs' Ringer bicarbonate solution (37°C, 95%, O2-5% CO2). Endothelium-independent contractions to KCl and prostaglandin F(2α) were unaltered after reperfusion. Endothelium-dependent relaxations to nitric oxide, sodium nitroprusside, and isoproterenol were comparable in control and reperfused arteries. However, reperfused coronary arteries contracted with prostaglandin F(2α) lost the ability to express endothelium-dependent relaxations to aggregating platelets. Reperfused arterial rings also exhibited impaired endothelium-dependent relaxations to acetylcholine, the calcium ionophore A23187, and the platelet-derived compounds ADP and serotonin. Quiescent (noncontracted) reperfused arterial rings exhibited larger conractions than controls when exposed to aggregating platelets. In such quiescent rings, the endothelium-dependent increase in tension to hemoglobin was unaltered after reperfusion. Thus, coronary reperfusion impairs the normal endothelium-dependent relaxations to aggregating platelets and vasoactive drugs. This impairment of platelet-mediated coronary relaxtion could help explain the increased vascular tone and tendency toward vasospasm commonly observed after reperfusion of the coronary arteries.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.orgen_US
dc.relation.ispartofCirculation Researchen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAdenosine Diphosphate - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCalcimycin - Pharmacologyen_US
dc.subject.meshCoronary Vessels - Drug Effects - Physiology - Physiopathologyen_US
dc.subject.meshDinoprost - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelium, Vascular - Physiology - Physiopathologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshHemoglobins - Pharmacologyen_US
dc.subject.meshIsoproterenol - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Physiology - Physiopathologyen_US
dc.subject.meshMyocardial Reperfusion Injury - Physiopathologyen_US
dc.subject.meshNitric Oxide - Pharmacologyen_US
dc.subject.meshPlatelet Aggregationen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshSerotonin - Pharmacologyen_US
dc.titleAcute impairment of endothelium-dependent relaxations to aggregating platelets following reperfusion injury in canine coronary arteriesen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid2115821-
dc.identifier.scopuseid_2-s2.0-0025365812en_US
dc.identifier.volume67en_US
dc.identifier.issue2en_US
dc.identifier.spage385en_US
dc.identifier.epage393en_US
dc.identifier.isiWOS:A1990DU14000015-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridPearson, PJ=7202175749en_US
dc.identifier.scopusauthoridSchaff, HV=36041155600en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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