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Article: Augmented endothelium-dependent constriction to hypoxia early and late following reperfusion of the canine coronary artery

TitleAugmented endothelium-dependent constriction to hypoxia early and late following reperfusion of the canine coronary artery
Authors
Issue Date1996
PublisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEP
Citation
Clinical And Experimental Pharmacology And Physiology, 1996, v. 23 n. 8, p. 634-641 How to Cite?
Abstract1. Canine coronary arteries with intact endothelium respond to hypoxaemia or serotonin infusion with dilatation, but when the endothelium is injured dysfunctional, these stimuli can cause constriction. The present studies investigated whether or not regional ischaemia and reperfusion alter endothelium-dependent responsiveness of canine coronary arteries in vivo and in vitro. 2. In organ chamber experiments, isolated control and reperfused coronary artery rings were contracted with prostaglandin F(2α) and exposed to hypoxia (PO2 less than 5 mmHg). 3. Hypoxia augmented the response of reperfused arteries more than that of controls. The hypoxic augmentation was blocked by N(G)-monomethyl-L-arginine, an inhibitor of nitric oxide synthesis from L-arginine. 4. These findings demonstrate that early following coronary reperfusion the hypoxic augmentation, which is mediated by a nitric oxide-dependent pathway in the endothelium, is facilitated. 5. In vivo studies revealed hyperconstriction of reperfused arteries in response to hypoxaemia (PO2 = 30-40 mmHg) and administration of either serotonin or ergonovine. 6. Twelve weeks following reperfusion injury, coronary arteries still exhibited augmented endothelium-dependent hypoxic augmentations in vitro, which were inhibited by N(G)-monomethyl-L-arginine. 7. Furthermore, resting coronary segments with endothelium displayed hypoxia-induced contractions that could not be inhibited by indomethacin, the lipoxygenase inhibitor AA861, superoxide dismutase plus catalase, deferoxamine, ouabain, or N(G)-monomethyl-L-arginine. 8. These endothelium-dependent hypoxic response may play a role in the pathogenesis of hyperconstriction (vasospasm) following coronary reperfusion.
Persistent Identifierhttp://hdl.handle.net/10722/171179
ISSN
2012 Impact Factor: 2.16
2015 SCImago Journal Rankings: 0.944
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorPearson, PJen_US
dc.contributor.authorLin, PJen_US
dc.contributor.authorSchaff, HVen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:33Z-
dc.date.available2012-10-30T06:12:33Z-
dc.date.issued1996en_US
dc.identifier.citationClinical And Experimental Pharmacology And Physiology, 1996, v. 23 n. 8, p. 634-641en_US
dc.identifier.issn0305-1870en_US
dc.identifier.urihttp://hdl.handle.net/10722/171179-
dc.description.abstract1. Canine coronary arteries with intact endothelium respond to hypoxaemia or serotonin infusion with dilatation, but when the endothelium is injured dysfunctional, these stimuli can cause constriction. The present studies investigated whether or not regional ischaemia and reperfusion alter endothelium-dependent responsiveness of canine coronary arteries in vivo and in vitro. 2. In organ chamber experiments, isolated control and reperfused coronary artery rings were contracted with prostaglandin F(2α) and exposed to hypoxia (PO2 less than 5 mmHg). 3. Hypoxia augmented the response of reperfused arteries more than that of controls. The hypoxic augmentation was blocked by N(G)-monomethyl-L-arginine, an inhibitor of nitric oxide synthesis from L-arginine. 4. These findings demonstrate that early following coronary reperfusion the hypoxic augmentation, which is mediated by a nitric oxide-dependent pathway in the endothelium, is facilitated. 5. In vivo studies revealed hyperconstriction of reperfused arteries in response to hypoxaemia (PO2 = 30-40 mmHg) and administration of either serotonin or ergonovine. 6. Twelve weeks following reperfusion injury, coronary arteries still exhibited augmented endothelium-dependent hypoxic augmentations in vitro, which were inhibited by N(G)-monomethyl-L-arginine. 7. Furthermore, resting coronary segments with endothelium displayed hypoxia-induced contractions that could not be inhibited by indomethacin, the lipoxygenase inhibitor AA861, superoxide dismutase plus catalase, deferoxamine, ouabain, or N(G)-monomethyl-L-arginine. 8. These endothelium-dependent hypoxic response may play a role in the pathogenesis of hyperconstriction (vasospasm) following coronary reperfusion.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEPen_US
dc.relation.ispartofClinical and Experimental Pharmacology and Physiologyen_US
dc.subject.meshAnalysis Of Varianceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCell Hypoxiaen_US
dc.subject.meshCoronary Angiographyen_US
dc.subject.meshCoronary Circulation - Drug Effects - Physiologyen_US
dc.subject.meshCoronary Vessels - Drug Effects - Physiologyen_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshIschemiaen_US
dc.subject.meshMyocardial Reperfusionen_US
dc.subject.meshNitric Oxide - Physiologyen_US
dc.subject.meshVasoconstriction - Physiologyen_US
dc.subject.meshOmega-N-Methylarginine - Pharmacologyen_US
dc.titleAugmented endothelium-dependent constriction to hypoxia early and late following reperfusion of the canine coronary arteryen_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.doi10.1111/j.1440-1681.1996.tb01749.x-
dc.identifier.pmid8886481-
dc.identifier.scopuseid_2-s2.0-0029846085en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0029846085&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume23en_US
dc.identifier.issue8en_US
dc.identifier.spage634en_US
dc.identifier.epage641en_US
dc.identifier.isiWOS:A1996VE53100002-
dc.publisher.placeAustraliaen_US
dc.identifier.scopusauthoridPearson, PJ=7202175749en_US
dc.identifier.scopusauthoridLin, PJ=7403224931en_US
dc.identifier.scopusauthoridSchaff, HV=36041155600en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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