Electrophysiology and neuronal integrity following systemic arterial hypotension in a rat model of unilateral carotid artery occlusion
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UMass Chan Affiliations
Department of NeurologyDocument Type
Journal ArticlePublication Date
2007-08-13Keywords
Analysis of VarianceAnimals
Carotid Stenosis
Cell Death
Cortical Spreading Depression
Disease Models, Animal
Electroencephalography
*Electrophysiology
Functional Laterality
Hypotension
Male
Neurons
Rats
Rats, Wistar
Reaction Time
Spectrum Analysis
Time Factors
Nervous System Diseases
Neurology
Neuroscience and Neurobiology
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Show full item recordAbstract
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.Source
Brain Res. 2007 Aug 13;1163:119-29. Epub 2007 Jun 16. Link to article on publisher's siteDOI
10.1016/j.brainres.2007.06.006Permanent Link to this Item
http://hdl.handle.net/20.500.14038/37770PubMed ID
17632088Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1016/j.brainres.2007.06.006