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Article: Alterations of mechanical properties in canine basilar arteries after subarachnoid hemorrhage

TitleAlterations of mechanical properties in canine basilar arteries 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. 71 n. 3, p. 430-436 How to Cite?
AbstractThe purpose of this study was to examine the hypotheses that structural stiffening of the arterial wall contributes to chronic cerebral vasospasm, and that alteration in properties of smooth muscle takes place after subarachnoid hemorrhage (SAH). Subarachnoid hemorrhage and subsequent chronic vasospasm were induced in dogs by two cisternal injections of autologous blood (on Day 0 and Day 2). Vasospasm was confirmed by angiography performed on Day 0 and Day 7. Animals in the control group underwent angiography only. On Day 8, the mechanical properties of the basilar arteries were studied in vitro. Passive compliance, measured under total inhibition of spontaneous myogenic tone with diltiazem (10 -4 M) plus papaverine (10 -4 M) was smaller in the SAH group. The length-contraction curve was shifted to the left and the optimum length for maximum contraction (L(max)) was significantly shorter in the spastic blood vessels. The spontaneous myogenic tone was augmented in the SAH group, resulting in an increase in resting tension at each length. By contrast, the maximum contractions in response to KCl and uridine 5'-triphosphate were markedly reduced in the SAH group, without changes in sensitivity to these agents. These differences in mechanical properties were observed in rings both with and without endothelium. The results indicate that, in chronic vasospasm, stiffening of the noncontractile component of the vasculature takes place as well as alterations in the contractile component, both of which presumably contribute to the shift in resting length-tension relationship and length-contraction relationship of the artery. The decreased distensibility, the increase in resting tension, and the shortening of the L(max) all favor a smaller diameter of the artery after SAH, possibly contributing to vasospasm.
Persistent Identifierhttp://hdl.handle.net/10722/170924
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.authorSundt Jr, TMen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:27Z-
dc.date.available2012-10-30T06:11:27Z-
dc.date.issued1989en_US
dc.identifier.citationJournal Of Neurosurgery, 1989, v. 71 n. 3, p. 430-436en_US
dc.identifier.issn0022-3085en_US
dc.identifier.urihttp://hdl.handle.net/10722/170924-
dc.description.abstractThe purpose of this study was to examine the hypotheses that structural stiffening of the arterial wall contributes to chronic cerebral vasospasm, and that alteration in properties of smooth muscle takes place after subarachnoid hemorrhage (SAH). Subarachnoid hemorrhage and subsequent chronic vasospasm were induced in dogs by two cisternal injections of autologous blood (on Day 0 and Day 2). Vasospasm was confirmed by angiography performed on Day 0 and Day 7. Animals in the control group underwent angiography only. On Day 8, the mechanical properties of the basilar arteries were studied in vitro. Passive compliance, measured under total inhibition of spontaneous myogenic tone with diltiazem (10 -4 M) plus papaverine (10 -4 M) was smaller in the SAH group. The length-contraction curve was shifted to the left and the optimum length for maximum contraction (L(max)) was significantly shorter in the spastic blood vessels. The spontaneous myogenic tone was augmented in the SAH group, resulting in an increase in resting tension at each length. By contrast, the maximum contractions in response to KCl and uridine 5'-triphosphate were markedly reduced in the SAH group, without changes in sensitivity to these agents. These differences in mechanical properties were observed in rings both with and without endothelium. The results indicate that, in chronic vasospasm, stiffening of the noncontractile component of the vasculature takes place as well as alterations in the contractile component, both of which presumably contribute to the shift in resting length-tension relationship and length-contraction relationship of the artery. The decreased distensibility, the increase in resting tension, and the shortening of the L(max) all favor a smaller diameter of the artery after SAH, possibly contributing to 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 - Pathology - Physiopathologyen_US
dc.subject.meshBiomechanicsen_US
dc.subject.meshDogsen_US
dc.subject.meshFemaleen_US
dc.subject.meshIschemic Attack, Transient - Etiology - Physiopathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshPotassium Chloride - Pharmacologyen_US
dc.subject.meshSubarachnoid Hemorrhage - Complications - Pathology - Physiopathologyen_US
dc.subject.meshUridine Triphosphate - Pharmacologyen_US
dc.subject.meshVasoconstriction - Drug Effectsen_US
dc.titleAlterations of mechanical properties in canine basilar arteries 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.1989.71.3.0430-
dc.identifier.pmid2769393-
dc.identifier.scopuseid_2-s2.0-0024374163en_US
dc.identifier.volume71en_US
dc.identifier.issue3en_US
dc.identifier.spage430en_US
dc.identifier.epage436en_US
dc.identifier.isiWOS:A1989AM28000017-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridKim, P=7402334666en_US
dc.identifier.scopusauthoridSundt Jr, TM=34572694400en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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