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Article: Recovery of endothelium-dependent relaxations four weeks after ischemia and progressive reperfusion in canine coronary arteries.

TitleRecovery of endothelium-dependent relaxations four weeks after ischemia and progressive reperfusion in canine coronary arteries.
Authors
Issue Date1996
PublisherBlackwell Publishing, Inc. The Journal's web site is located at http://www.blackwell-science.com
Citation
Proceedings Of The Association Of American Physicians, 1996, v. 108 n. 5, p. 362-367 How to Cite?
AbstractThe acute impairment of endothelium-dependent relaxations after ischemia and acute reperfusion injury has been studied extensively. However, less is known about the chronic status of the coronary endothelium following progressive reperfusion. Experiments were designed to characterize, after 60 min of ischemia followed by progressive reperfusion, the coronary endothelial function under acute and chronic conditions. Heartworm-free mongrel dogs were used. A percutaneous balloon catheter was inflated to occlude the left anterior descending coronary artery for 60 min, followed by progressive deflation. After 60 min or 4 weeks of reperfusion, the coronary arteries were dissected free, cut into rings, suspended in organ chambers, and exposed to endothelium-dependent and endothelium-independent agonists, both in the presence and absence of pertussis toxin. Left circumflex coronary arteries (from the same dogs) that had not been subjected to occlusion and reperfusion were studied in parallel as controls. The acute endothelium-dependent relaxations to serotonin, thrombin, and adenosine/diphosphate were impaired significantly following ischemia-reperfusion injury. Four weeks after ischemia-reperfusion injury, the endothelium-dependent relaxations to these substances were normal compared with those of controls. The endothelium-dependent relaxations to acetylcholine, bradykinin, and the calcium ionophore A23187 were unaffected either acutely or chronically. An early impairment of endothelium-dependent relaxations after ischemia-reperfusion injury occurs in response to serotonin, thrombin, and adenosine diphosphate. This early impairment is transient and is not evident 4 weeks after reperfusion. In contrast to the regenerated endothelium following balloon deendothelialization, the chronic endothelial pertussis toxin-sensitive G-protein function is not impaired selectively after ischemia-reperfusion injury, provided the reperfusion occurs gradually.
Persistent Identifierhttp://hdl.handle.net/10722/171190
ISSN
2001 Impact Factor: 4.797
2002 SCImago Journal Rankings: 1.427
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLee, JJen_US
dc.contributor.authorOlmos, Len_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:36Z-
dc.date.available2012-10-30T06:12:36Z-
dc.date.issued1996en_US
dc.identifier.citationProceedings Of The Association Of American Physicians, 1996, v. 108 n. 5, p. 362-367en_US
dc.identifier.issn1081-650Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/171190-
dc.description.abstractThe acute impairment of endothelium-dependent relaxations after ischemia and acute reperfusion injury has been studied extensively. However, less is known about the chronic status of the coronary endothelium following progressive reperfusion. Experiments were designed to characterize, after 60 min of ischemia followed by progressive reperfusion, the coronary endothelial function under acute and chronic conditions. Heartworm-free mongrel dogs were used. A percutaneous balloon catheter was inflated to occlude the left anterior descending coronary artery for 60 min, followed by progressive deflation. After 60 min or 4 weeks of reperfusion, the coronary arteries were dissected free, cut into rings, suspended in organ chambers, and exposed to endothelium-dependent and endothelium-independent agonists, both in the presence and absence of pertussis toxin. Left circumflex coronary arteries (from the same dogs) that had not been subjected to occlusion and reperfusion were studied in parallel as controls. The acute endothelium-dependent relaxations to serotonin, thrombin, and adenosine/diphosphate were impaired significantly following ischemia-reperfusion injury. Four weeks after ischemia-reperfusion injury, the endothelium-dependent relaxations to these substances were normal compared with those of controls. The endothelium-dependent relaxations to acetylcholine, bradykinin, and the calcium ionophore A23187 were unaffected either acutely or chronically. An early impairment of endothelium-dependent relaxations after ischemia-reperfusion injury occurs in response to serotonin, thrombin, and adenosine diphosphate. This early impairment is transient and is not evident 4 weeks after reperfusion. In contrast to the regenerated endothelium following balloon deendothelialization, the chronic endothelial pertussis toxin-sensitive G-protein function is not impaired selectively after ischemia-reperfusion injury, provided the reperfusion occurs gradually.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing, Inc. The Journal's web site is located at http://www.blackwell-science.comen_US
dc.relation.ispartofProceedings of the Association of American Physiciansen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAdenosine Diphosphate - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArteries - Physiologyen_US
dc.subject.meshBradykinin - Pharmacologyen_US
dc.subject.meshCoronary Vessels - Physiologyen_US
dc.subject.meshDogsen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshMaleen_US
dc.subject.meshMolsidomine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshMuscle Relaxation - Physiologyen_US
dc.subject.meshReperfusion Injuryen_US
dc.subject.meshSerotonin - Pharmacologyen_US
dc.subject.meshThrombin - Pharmacologyen_US
dc.subject.meshTime Factorsen_US
dc.titleRecovery of endothelium-dependent relaxations four weeks after ischemia and progressive reperfusion in canine coronary arteries.en_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.pmid8902880-
dc.identifier.scopuseid_2-s2.0-0030225865en_US
dc.identifier.volume108en_US
dc.identifier.issue5en_US
dc.identifier.spage362en_US
dc.identifier.epage367en_US
dc.identifier.isiWOS:A1996VP84500003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLee, JJ=7601457545en_US
dc.identifier.scopusauthoridOlmos, L=7005286818en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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