Long‐term measurement of cerebral blood flow and metabolism in a rat chronic hypoperfusion model

Abstract

1. Rat bilateral common carotid artery occlusion (BCAO) was used as a chronic cerebral hypoperfusion model. We observed autoradiographically the long-term changes in regional cerebral blood flow (rCBF) and regional cerebral glucose utilization (rCGU) after 2 days and 1, 4 and 8 weeks of BCAO and in controls. Regions evaluated included the cerebral cortex, white matter and basal ganglia. Pathological changes were also observed with Klüver-Barrera and haematoxylin-eosin staining. 2. After 2 days, rCBF was significantly reduced to 33-58% in the cortex, white matter and amygdala and similar reductions were observed after 1 week. 3. After 4 weeks, rCBF recovered; however, rCBF remained significantly reduced in the occipital cortex, white matter, globus pallidus and substantia nigra. 4. After 2 days, rCGU was mostly maintained but, after 1 week, rCGU was reduced significantly to 40-70% in the cortex, white matter, basal ganglia and thalamus. Four weeks later, these reductions were no longer seen. 5. Rarefaction of the white matter was observed from 1 week. 6. These results showed that the BCAO in rats is an appropriate model for chronic cerebral hypoperfusion and that uncoupling of rCBF and rCGU was observed from 2 days until 4 weeks in the white matter.

Ceftriaxone improves spatial learning and memory in chronic cerebral hypoperfused rats

“…Some studies showed increased uptake activity without transporter protein level changes 28 . CBF gradually increases after initial drop immediately after arterial ligation to reach approximately 70% of control rats within 8 weeks to 3 months 50,51 . Therefore, the GLT-1 expression might also depend on the duration after cerebral hypoperfusion.…”

The neuron-astrocyte-microglia triad in CA3 after chronic cerebral hypoperfusion in the rat: Protective effect of dipyridamole

“…In this research we used the model of brain chronic hypoperfusion with the permanent bilateral common carotid artery occlusion or two vessel occlusion (2VO) in the rat (Sarti et al 2002a(Sarti et al , 2002bFarkas et al 2007;Lana et al 2014), a suitable animal species for this purpose since the circle of Willis affords reduced blood flow to the brain (Otori et al 2003). As outlined by Farkas et al (2007) the rat 2VO model is useful to investigate the long-term effects of chronic cerebral hypoperfusion (Farkas et al 2007) since hypoperfusion is global although mild, and represents a model of cerebrovascular stenosis in aging humans.…”

Cerebrovascular dysfunction and microcirculation rarefaction precede white matter lesions in a mouse genetic model of cerebral ischemic small vessel disease

“…CBF studies in human patients have documented hypoperfusion in the white matter within regions of leukoaraiosis as well as, to a lesser extent, in the normal-appearing white matter (41). Experimental studies in rodents have demonstrated that chronic brain hypoperfusion, induced by permanent ligation or stenosis of both common carotid arteries, produced lesions located predominantly in the white matter, with vacuolation, astrogliosis, and demyelination (2,42,43). Importantly, studies in the mouse in which the level of hypoperfusion was controlled by adjusting the internal diameter of microcoils placed around the carotid arteries provided evidence that the magnitude of hypoperfusion determined the ratio of white versus gray matter injury.…”