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Article: Release of endothelium-derived relaxing factor after subarachnoid hemorrhage.

TitleRelease of endothelium-derived relaxing factor after subarachnoid hemorrhage.
Authors
Issue Date1989
PublisherAmerican Association of Neurological Surgeons. The Journal's web site is located at http://www.thejns-net.org
Citation
Journal Of Neurosurgery, 1989, v. 70 n. 1, p. 108-114 How to Cite?
AbstractThe purpose of this study was to determine the cause of the loss of endothelium-dependent relaxation observed in chronic cerebral vasospasm. A bioassay system was developed to measure the release of endothelium-derived relaxing factor (EDRF) from canine basilar arteries. Subarachnoid hemorrhage (SAH) was induced in dogs by two injections of autologous blood into the cisterna magna. Angiograms were performed on the 7th day after SAH to check the presence of chronic vasospasm. The animals were sacrificed on the 8th day, and in vitro experiments were performed on rings harvested from the basilar artery. These confirmed loss of endothelium-dependent relaxation in response to bradykinin and arginine vasopressin in the group with SAH. The basilar arteries were perfused with modified Krebs-Ringer solution. The perfusate was bioassayed with a ring of coronary artery without endothelium (bioassay ring). The release of the EDRF was detected by relaxation of the bioassay ring contracted with prostaglandin F2 alpha. Arginine vasopressin and bradykinin added to the perfusate upstream of the basilar artery caused concentration-dependent release of the EDRF. The direct effect of these peptides on the smooth muscle of the bioassay ring was to cause contraction. The release of the EDRF was identical in basilar arteries from the control and the SAH groups. These results indicate that the release of the EDRF is not impaired during chronic vasospasm, and thus that the loss of the endothelium-dependent relaxation is due to a decreased transfer of the EDRF or a reduced responsiveness of the smooth muscle to the factor.
Persistent Identifierhttp://hdl.handle.net/10722/170946
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.authorLorenz, RRen_US
dc.contributor.authorSundt Jr, TMen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:33Z-
dc.date.available2012-10-30T06:11:33Z-
dc.date.issued1989en_US
dc.identifier.citationJournal Of Neurosurgery, 1989, v. 70 n. 1, p. 108-114en_US
dc.identifier.issn0022-3085en_US
dc.identifier.urihttp://hdl.handle.net/10722/170946-
dc.description.abstractThe purpose of this study was to determine the cause of the loss of endothelium-dependent relaxation observed in chronic cerebral vasospasm. A bioassay system was developed to measure the release of endothelium-derived relaxing factor (EDRF) from canine basilar arteries. Subarachnoid hemorrhage (SAH) was induced in dogs by two injections of autologous blood into the cisterna magna. Angiograms were performed on the 7th day after SAH to check the presence of chronic vasospasm. The animals were sacrificed on the 8th day, and in vitro experiments were performed on rings harvested from the basilar artery. These confirmed loss of endothelium-dependent relaxation in response to bradykinin and arginine vasopressin in the group with SAH. The basilar arteries were perfused with modified Krebs-Ringer solution. The perfusate was bioassayed with a ring of coronary artery without endothelium (bioassay ring). The release of the EDRF was detected by relaxation of the bioassay ring contracted with prostaglandin F2 alpha. Arginine vasopressin and bradykinin added to the perfusate upstream of the basilar artery caused concentration-dependent release of the EDRF. The direct effect of these peptides on the smooth muscle of the bioassay ring was to cause contraction. The release of the EDRF was identical in basilar arteries from the control and the SAH groups. These results indicate that the release of the EDRF is not impaired during chronic vasospasm, and thus that the loss of the endothelium-dependent relaxation is due to a decreased transfer of the EDRF or a reduced responsiveness of the smooth muscle to the factor.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 - Metabolism - Physiopathology - Radiographyen_US
dc.subject.meshBiological Assayen_US
dc.subject.meshBiological Factors - Metabolismen_US
dc.subject.meshCerebral Angiographyen_US
dc.subject.meshDogsen_US
dc.subject.meshFemaleen_US
dc.subject.meshMaleen_US
dc.subject.meshNitric Oxideen_US
dc.subject.meshSubarachnoid Hemorrhage - Metabolism - Physiopathology - Radiographyen_US
dc.subject.meshVasodilationen_US
dc.titleRelease of endothelium-derived relaxing factor after subarachnoid hemorrhage.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.doi10.3171/jns.1989.70.1.0108-
dc.identifier.pmid2783340-
dc.identifier.scopuseid_2-s2.0-0024484899en_US
dc.identifier.volume70en_US
dc.identifier.issue1en_US
dc.identifier.spage108en_US
dc.identifier.epage114en_US
dc.identifier.isiWOS:A1989R555400019-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridKim, P=7402334666en_US
dc.identifier.scopusauthoridLorenz, RR=7402095192en_US
dc.identifier.scopusauthoridSundt Jr, TM=34572694400en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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