Abstract
We investigated the chronic effects of cerebral hypoperfusion on neuronal density and functional hyperemia using our misery perfusion mouse model under unilateral common carotid artery occlusion (UCCAO). Neuronal density evaluated 28 days after UCCAO using [11C]flumazenil-PET and histology indicated no neurologic deficit in the hippocampus and neocortex. CBF response to sensory stimulation was assessed using laser-Doppler flowmetry. Percentage changes in CBF response of the ipsilateral hemisphere to UCCAO were 18.4 ± 3.0%, 6.9 ± 2.8%, 6.8 ± 2.3% and 4.9 ± 2.4% before, and 7, 14 and 28 days after UCCAO, respectively. Statistical significance was found at 7, 14 and 28 days after UCCAO (P < 0.01). Contrary to our previous finding (Tajima et al. 2014) showing recovered CBF response to hypercapnia on 28 days after UCCAO using the same model, functional hyperemia was sustained and became worse 28 days after UCCAO.
Highlights
Permanent UCCAO showed a chronic mild decrease in Cerebral blood flow (CBF) and a decrease in the CBF response to hypercapnia, this indicated that misery perfusion occurred in our animal model[10]
chronic cerebral hypoperfusion (CCH) leads to a decline of cognitive functions in animals subjected to either UCCAO or BCCAO8,9, indicating that CCH-triggered cognitive dysfunction is closely associated with neurologic deficits or neural dysfunctions
Our results of [11C]FMZ-positron emission tomography (PET), structural MRI, and immunohistochemistry examinations all consistently showed that neither neurologic deficit nor brain atrophy was observed in the neocortex and hippocampus after one month of CCH (Figs 3–5), which was quite contrary to our expectation
Summary
Permanent UCCAO showed a chronic mild decrease in CBF and a decrease in the CBF response to hypercapnia, this indicated that misery perfusion occurred in our animal model[10]. Previous studies have demonstrated that CCH causes white matter lesion and attenuation of cognitive function, suggesting morphological and functional damage of brain cells under misery perfusion. We investigated whether neurological deficit, brain atrophy and reduction of functional hyperemia occurred in the mouse model of misery perfusion. To estimate neurological deficit and brain atrophy, [11C]flumazenil ([11C]FMZ) positron emission tomography (PET) and histology were performed with our mouse model. Our results showed selective impairment of functional hyperemia, associated with CCH in the animal model of misery perfusion
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