Title

Electrophysiology and neuronal integrity following systemic arterial hypotension in a rat model of unilateral carotid artery occlusion

UMMS Affiliation

Department of Neurology

Publication Date

2007-08-13

Document Type

Article

Subjects

Analysis of Variance; Animals; 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

Disciplines

Nervous System Diseases | Neurology | Neuroscience and Neurobiology

Abstract

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.

DOI of Published Version

10.1016/j.brainres.2007.06.006

Source

Brain Res. 2007 Aug 13;1163:119-29. Epub 2007 Jun 16. Link to article on publisher's site

Journal/Book/Conference Title

Brain research

Related Resources

Link to Article in PubMed

PubMed ID

17632088

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