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Article: The effect of hypothermic ischemia on the α-adrenergic mechanisms of the canine tibia vascular bed

TitleThe effect of hypothermic ischemia on the α-adrenergic mechanisms of the canine tibia vascular bed
Authors
Issue Date1992
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.elsevier.com/locate/orthres
Citation
Journal Of Orthopaedic Research, 1992, v. 10 n. 1, p. 149-155 How to Cite?
AbstractThe effect of hypothermic ischemia on α-1 and -2 adrenergic receptor mediated vasoconstriction has been studied in an in vitro perfused canine tibia preparation. Bones were perfused at a constant rate with aerated (95% O2, 5% CO2) modified Krebs Ringer solution and the effect of bolus injections of norepinephrine (0.025-6.4 nmol) on the perfusion pressure was studied. For all bones the first dose-response curve was produced under control conditions. In one group the second dose-response curve was generated during a constant infusion of prazosin (α-1 adrenergic antagonist); in another it was produced during a constant infusion of rauwolscine (α-2 adrenergic antagonist); in the control group it was generated under control conditions. The results demonstrate that, after 48 h of hypothermic ischemia, α-1 adrenergic-mediated vasoconstriction was significantly attenuated (p < 0.001). However, α-2 adrenergic-mediated vasoconstriction was unaffected by increasing periods of hypothermic ischemia. | The effect of hypothermic ischemia on α-1 and -2 adrenergic receptor mediated vasoconstriction has been studied in an in vitro perfused canine tibia preparation. Bones were perfused at a constant rate with aerated (95% O2, 5% CO2) modified Krebs Ringer solution and the effect of bolus injections of norepinephrine (0.025-6.4 nmol) on the perfusion pressure was studied. For all bones the first dose-response curve was produced under control conditions. In one group the second dose-response curve was generated during a constant infusion of prazosin (α-1 adrenergic antagonist); in another it was produced during a constant infusion of rauwolscine (α-2 adrenergic antagonist); in the control group it was generated under control conditions. The results demonstrate that, after 48 h of hypothermic ischemia, α-1 adrenergic-mediated vasoconstriction was significantly attenuated (p < 0.001). However, α-2 adrenergic-mediated vasoconstriction was unaffected by increasing periods of hypothermic ischemia.
Persistent Identifierhttp://hdl.handle.net/10722/171050
ISSN
2015 Impact Factor: 2.807
2015 SCImago Journal Rankings: 1.464
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDavis, TRCen_US
dc.contributor.authorWood, MBen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:59Z-
dc.date.available2012-10-30T06:11:59Z-
dc.date.issued1992en_US
dc.identifier.citationJournal Of Orthopaedic Research, 1992, v. 10 n. 1, p. 149-155en_US
dc.identifier.issn0736-0266en_US
dc.identifier.urihttp://hdl.handle.net/10722/171050-
dc.description.abstractThe effect of hypothermic ischemia on α-1 and -2 adrenergic receptor mediated vasoconstriction has been studied in an in vitro perfused canine tibia preparation. Bones were perfused at a constant rate with aerated (95% O2, 5% CO2) modified Krebs Ringer solution and the effect of bolus injections of norepinephrine (0.025-6.4 nmol) on the perfusion pressure was studied. For all bones the first dose-response curve was produced under control conditions. In one group the second dose-response curve was generated during a constant infusion of prazosin (α-1 adrenergic antagonist); in another it was produced during a constant infusion of rauwolscine (α-2 adrenergic antagonist); in the control group it was generated under control conditions. The results demonstrate that, after 48 h of hypothermic ischemia, α-1 adrenergic-mediated vasoconstriction was significantly attenuated (p < 0.001). However, α-2 adrenergic-mediated vasoconstriction was unaffected by increasing periods of hypothermic ischemia. | The effect of hypothermic ischemia on α-1 and -2 adrenergic receptor mediated vasoconstriction has been studied in an in vitro perfused canine tibia preparation. Bones were perfused at a constant rate with aerated (95% O2, 5% CO2) modified Krebs Ringer solution and the effect of bolus injections of norepinephrine (0.025-6.4 nmol) on the perfusion pressure was studied. For all bones the first dose-response curve was produced under control conditions. In one group the second dose-response curve was generated during a constant infusion of prazosin (α-1 adrenergic antagonist); in another it was produced during a constant infusion of rauwolscine (α-2 adrenergic antagonist); in the control group it was generated under control conditions. The results demonstrate that, after 48 h of hypothermic ischemia, α-1 adrenergic-mediated vasoconstriction was significantly attenuated (p < 0.001). However, α-2 adrenergic-mediated vasoconstriction was unaffected by increasing periods of hypothermic ischemia.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.elsevier.com/locate/orthresen_US
dc.relation.ispartofJournal of Orthopaedic Researchen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlood Vessels - Innervationen_US
dc.subject.meshDogsen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshHypothermia - Physiopathologyen_US
dc.subject.meshIschemia - Physiopathologyen_US
dc.subject.meshNorepinephrine - Pharmacologyen_US
dc.subject.meshPerfusionen_US
dc.subject.meshPressureen_US
dc.subject.meshReceptors, Adrenergic, Alpha - Physiologyen_US
dc.subject.meshRegional Blood Flowen_US
dc.subject.meshTibia - Blood Supplyen_US
dc.subject.meshYohimbine - Pharmacologyen_US
dc.titleThe effect of hypothermic ischemia on the α-adrenergic mechanisms of the canine tibia vascular beden_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.doi10.1002/jor.1100100118-
dc.identifier.pmid1309385-
dc.identifier.scopuseid_2-s2.0-0026546866en_US
dc.identifier.volume10en_US
dc.identifier.issue1en_US
dc.identifier.spage149en_US
dc.identifier.epage155en_US
dc.identifier.isiWOS:A1992GX48200017-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridDavis, TRC=8642707500en_US
dc.identifier.scopusauthoridWood, MB=7403448994en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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