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

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 (H&E) 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 ∼ 6-10%) and amplitudes (by ∼ 57-70%), and induced selective neuronal cell death in the cerebral cortex and hippocampus (P < 0.05 vs. contralateral). Spontaneous CSD occurred in ∼ 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.