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Article: Alterations in endothelium-dependent responsiveness of the canine basilar artery after subarachnoid hemorrhage

TitleAlterations in endothelium-dependent responsiveness of the canine basilar artery after subarachnoid hemorrhage
Authors
Issue Date1988
PublisherAmerican Association of Neurological Surgeons. The Journal's web site is located at http://www.thejns-net.org
Citation
Journal Of Neurosurgery, 1988, v. 69 n. 2, p. 239-246 How to Cite?
AbstractTo investigate the alteration of endothelium-dependent responses in chronic vasospasm after subarachnoid hemorrhage (SAH), experiments were carried out in the double-hemorrhage canine model. After the presence of vasospasm was confirmed by cerebral angiography on Day 0 and 7, pharmacological studies on the basilar artery were conducted in vitro on Day 8. In the SAH group, endothelium-dependent relaxation was abolished in response to arginine vasopressin and was significantly reduced in response to thrombin. Endothelium-independent relaxation in the SAH group was preserved in response to papaverine and was minimally reduced in response to sodium nitroprusside. Endothelium-dependent contraction in response to arachidonic acid, acetylcholine, the calcium ionophore A23187, adenosine diphosphate, mechanical stretching, and hypoxia persisted in the SAH group. The maximal contraction to KCl and uridine triphosphate, which is endothelium-independent, was diminished in the SAH group, but no changes in sensitivity were noted in the concentration-response relationships. A significant correlation was observed between the degree of vasospasm determined angiographically and the loss of endothelium-dependent relaxation. The loss of endothelium-dependent relaxation and the persistence of endothelium-dependent contraction suggest that the deterioration in the endothelium-dependent responses may be an important component in the pathogenesis of cerebral vasospasm.
Persistent Identifierhttp://hdl.handle.net/10722/170871
ISSN
2015 Impact Factor: 3.443
2015 SCImago Journal Rankings: 1.673
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorKim, Pen_US
dc.contributor.authorSunte Jr, TMen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:12Z-
dc.date.available2012-10-30T06:11:12Z-
dc.date.issued1988en_US
dc.identifier.citationJournal Of Neurosurgery, 1988, v. 69 n. 2, p. 239-246en_US
dc.identifier.issn0022-3085en_US
dc.identifier.urihttp://hdl.handle.net/10722/170871-
dc.description.abstractTo investigate the alteration of endothelium-dependent responses in chronic vasospasm after subarachnoid hemorrhage (SAH), experiments were carried out in the double-hemorrhage canine model. After the presence of vasospasm was confirmed by cerebral angiography on Day 0 and 7, pharmacological studies on the basilar artery were conducted in vitro on Day 8. In the SAH group, endothelium-dependent relaxation was abolished in response to arginine vasopressin and was significantly reduced in response to thrombin. Endothelium-independent relaxation in the SAH group was preserved in response to papaverine and was minimally reduced in response to sodium nitroprusside. Endothelium-dependent contraction in response to arachidonic acid, acetylcholine, the calcium ionophore A23187, adenosine diphosphate, mechanical stretching, and hypoxia persisted in the SAH group. The maximal contraction to KCl and uridine triphosphate, which is endothelium-independent, was diminished in the SAH group, but no changes in sensitivity were noted in the concentration-response relationships. A significant correlation was observed between the degree of vasospasm determined angiographically and the loss of endothelium-dependent relaxation. The loss of endothelium-dependent relaxation and the persistence of endothelium-dependent contraction suggest that the deterioration in the endothelium-dependent responses may be an important component in the pathogenesis of cerebral vasospasm.en_US
dc.languageengen_US
dc.publisherAmerican Association of Neurological Surgeons. The Journal's web site is located at http://www.thejns-net.orgen_US
dc.relation.ispartofJournal of Neurosurgeryen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBasilar Artery - Drug Effects - Physiologyen_US
dc.subject.meshBiological Agents - Physiologyen_US
dc.subject.meshCalcimycin - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEndothelium - Drug Effects - Physiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshIschemic Attack, Transient - Metabolism - Physiopathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshNitric Oxideen_US
dc.subject.meshNitroprusside - Pharmacologyen_US
dc.subject.meshSubarachnoid Hemorrhage - Metabolism - Physiopathologyen_US
dc.subject.meshVasoconstrictionen_US
dc.subject.meshVasodilationen_US
dc.titleAlterations in endothelium-dependent responsiveness of the canine basilar artery after subarachnoid hemorrhageen_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.doi10.3171/jns.1988.69.2.0239-
dc.identifier.pmid3134520-
dc.identifier.scopuseid_2-s2.0-0023720307en_US
dc.identifier.volume69en_US
dc.identifier.issue2en_US
dc.identifier.spage239en_US
dc.identifier.epage246en_US
dc.identifier.isiWOS:A1988P400500014-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridKim, P=7402334666en_US
dc.identifier.scopusauthoridSunte Jr, TM=6503913958en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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