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dc.contributor.authorHenninger, Nils
dc.contributor.authorHeimann, Axel
dc.contributor.authorKempski, Oliver
dc.date2022-08-11T08:09:28.000
dc.date.accessioned2022-08-23T16:31:56Z
dc.date.available2022-08-23T16:31:56Z
dc.date.issued2007-08-13
dc.date.submitted2016-05-10
dc.identifier.citationBrain Res. 2007 Aug 13;1163:119-29. Epub 2007 Jun 16. <a href="http://dx.doi.org/10.1016/j.brainres.2007.06.006">Link to article on publisher's site</a>
dc.identifier.issn0006-8993 (Linking)
dc.identifier.doi10.1016/j.brainres.2007.06.006
dc.identifier.pmid17632088
dc.identifier.urihttp://hdl.handle.net/20.500.14038/37770
dc.description.abstractPatients with carotid artery stenosis may be particularly susceptible to hypotension-associated cerebral ischemia and subsequent neurological sequelae. Measuring somatosensory evoked potentials (SEP), electroencephalogram (EEG), direct current (DC) potential, and histology, we compared the temporal evolution of cortical functional perturbations as well as neuronal integrity in a model of unilateral carotid artery occlusion and systemic hypobaric hypotension (HH) at the lower limit of cerebral blood flow autoregulation (50 mm Hg). Serial measurements of EEG power spectra as well as SEP-amplitudes and latencies of N10.3 were performed before, during, and up to 60 min after 30 min-HH (n=7) or the control condition (n=7) in male Wistar rats. In two additional groups (with [n=7] or without [n=7] HH), cortical spreading depressions (CSD) were elicited to ascertain their contribution to brain injury. Hematoxilin-Eosin (HandE) staining was used to assess neuronal cell death at 5 days after surgery. Relative to baseline, HH attenuated ipsilateral EEG power spectrum (by maximally 62%), increased SEP-latencies (by approximately 6-10%) and amplitudes (by approximately 57-70%), and induced selective neuronal cell death in the cerebral cortex and hippocampus (P < 0.05 vs. contralateral). Spontaneous CSD occurred in approximately 30% of HH-animals. Repolarization of the DC-potential during HH was significantly prolonged relative to normotensive conditions (10.3+/-11.5 min, P < 0.001). Our model may help to understand underlying pathophysiology and improve outcome in a clinical subset of patients with carotid artery stenosis and transient systemic hypotension.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=17632088&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1016/j.brainres.2007.06.006
dc.subjectAnalysis of Variance
dc.subjectAnimals
dc.subjectCarotid Stenosis
dc.subjectCell Death
dc.subjectCortical Spreading Depression
dc.subjectDisease Models, Animal
dc.subjectElectroencephalography
dc.subject*Electrophysiology
dc.subjectFunctional Laterality
dc.subjectHypotension
dc.subjectMale
dc.subjectNeurons
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectReaction Time
dc.subjectSpectrum Analysis
dc.subjectTime Factors
dc.subjectNervous System Diseases
dc.subjectNeurology
dc.subjectNeuroscience and Neurobiology
dc.titleElectrophysiology and neuronal integrity following systemic arterial hypotension in a rat model of unilateral carotid artery occlusion
dc.typeJournal Article
dc.source.journaltitleBrain research
dc.source.volume1163
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/neuro_pp/450
dc.identifier.contextkey8585909
html.description.abstract<p>Patients with carotid artery stenosis may be particularly susceptible to hypotension-associated cerebral ischemia and subsequent neurological sequelae. Measuring somatosensory evoked potentials (SEP), electroencephalogram (EEG), direct current (DC) potential, and histology, we compared the temporal evolution of cortical functional perturbations as well as neuronal integrity in a model of unilateral carotid artery occlusion and systemic hypobaric hypotension (HH) at the lower limit of cerebral blood flow autoregulation (50 mm Hg). Serial measurements of EEG power spectra as well as SEP-amplitudes and latencies of N10.3 were performed before, during, and up to 60 min after 30 min-HH (n=7) or the control condition (n=7) in male Wistar rats. In two additional groups (with [n=7] or without [n=7] HH), cortical spreading depressions (CSD) were elicited to ascertain their contribution to brain injury. Hematoxilin-Eosin (HandE) staining was used to assess neuronal cell death at 5 days after surgery. Relative to baseline, HH attenuated ipsilateral EEG power spectrum (by maximally 62%), increased SEP-latencies (by approximately 6-10%) and amplitudes (by approximately 57-70%), and induced selective neuronal cell death in the cerebral cortex and hippocampus (P < 0.05 vs. contralateral). Spontaneous CSD occurred in approximately 30% of HH-animals. Repolarization of the DC-potential during HH was significantly prolonged relative to normotensive conditions (10.3+/-11.5 min, P < 0.001). Our model may help to understand underlying pathophysiology and improve outcome in a clinical subset of patients with carotid artery stenosis and transient systemic hypotension.</p>
dc.identifier.submissionpathneuro_pp/450
dc.contributor.departmentDepartment of Neurology
dc.source.pages119-29


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