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- Publisher Website: 10.3171/jns.1989.70.1.0108
- Scopus: eid_2-s2.0-0024484899
- PMID: 2783340
- WOS: WOS:A1989R555400019
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Article: Release of endothelium-derived relaxing factor after subarachnoid hemorrhage.
Title | Release of endothelium-derived relaxing factor after subarachnoid hemorrhage. |
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Authors | |
Issue Date | 1989 |
Publisher | American 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? |
Abstract | The 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 Identifier | http://hdl.handle.net/10722/170946 |
ISSN | 2023 Impact Factor: 3.5 2023 SCImago Journal Rankings: 1.173 |
ISI Accession Number ID |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, P | en_US |
dc.contributor.author | Lorenz, RR | en_US |
dc.contributor.author | Sundt Jr, TM | en_US |
dc.contributor.author | Vanhoutte, PM | en_US |
dc.date.accessioned | 2012-10-30T06:11:33Z | - |
dc.date.available | 2012-10-30T06:11:33Z | - |
dc.date.issued | 1989 | en_US |
dc.identifier.citation | Journal Of Neurosurgery, 1989, v. 70 n. 1, p. 108-114 | en_US |
dc.identifier.issn | 0022-3085 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/170946 | - |
dc.description.abstract | The 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.language | eng | en_US |
dc.publisher | American Association of Neurological Surgeons. The Journal's web site is located at http://www.thejns-net.org | en_US |
dc.relation.ispartof | Journal of Neurosurgery | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Basilar Artery - Metabolism - Physiopathology - Radiography | en_US |
dc.subject.mesh | Biological Assay | en_US |
dc.subject.mesh | Biological Factors - Metabolism | en_US |
dc.subject.mesh | Cerebral Angiography | en_US |
dc.subject.mesh | Dogs | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Nitric Oxide | en_US |
dc.subject.mesh | Subarachnoid Hemorrhage - Metabolism - Physiopathology - Radiography | en_US |
dc.subject.mesh | Vasodilation | en_US |
dc.title | Release of endothelium-derived relaxing factor after subarachnoid hemorrhage. | en_US |
dc.type | Article | en_US |
dc.identifier.email | Vanhoutte, PM:vanhoutt@hku.hk | en_US |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.3171/jns.1989.70.1.0108 | - |
dc.identifier.pmid | 2783340 | - |
dc.identifier.scopus | eid_2-s2.0-0024484899 | en_US |
dc.identifier.volume | 70 | en_US |
dc.identifier.issue | 1 | en_US |
dc.identifier.spage | 108 | en_US |
dc.identifier.epage | 114 | en_US |
dc.identifier.isi | WOS:A1989R555400019 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Kim, P=7402334666 | en_US |
dc.identifier.scopusauthorid | Lorenz, RR=7402095192 | en_US |
dc.identifier.scopusauthorid | Sundt Jr, TM=34572694400 | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.issnl | 0022-3085 | - |