Systematic comparison of basic animal models of cerebral hypoperfusion

Anti-Inflammatory Effect of Beta-Caryophyllene Mediated by the Involvement of TRPV1, BDNF and trkB in the Rat Cerebral Cortex after Hypoperfusion/Reperfusion

“…The transient BCCAO model is the most employed model of global cerebral hypoperfusion that can be adapted to investigate the efficacy of therapies in acute vascular accidents when the revascularization leads to the pathophysiological sequelae of reperfusion [ 5 , 61 ]. The BCCAO model, despite the blood flow compensation due to the circle of Willis, has been reported in the rat to cause a reduction of cerebral blood flow of 25 to 87% (depending on the brain region examined), amounting to about 63% in the frontal cortex to about 20% in the hippocampus vs. sham animals after 2.5 h of arterial ligation [ 13 ].…”

“…Accumulating evidence shows that inflammation plays a crucial role in the pathogenesis of cerebral ischemia and represents a target for promising therapeutic intervention [ 1 , 2 ]. While the severity and treatment of ischemia-induced functional and metabolic dysregulation depend on various factors [ 3 , 4 , 5 ]—the vessel occluded, permanent or temporary hypoperfusion, the timing of intervention—preventive strategies to reduce the risk factors for ischemic stroke, such as carotid artery stenosis, have extensively gained attention from researchers [ 6 ]. The knowledge accrued from the utilization of preclinical models of cerebral hypoperfusion/revascularization injury [ 5 ] has allowed not only to identify the nature and dynamics of the reperfusion injury [ 1 , 6 , 7 , 8 ] but also to correlate hypoperfusion/reperfusion to reliable biomarker changes.…”

“…While the severity and treatment of ischemia-induced functional and metabolic dysregulation depend on various factors [ 3 , 4 , 5 ]—the vessel occluded, permanent or temporary hypoperfusion, the timing of intervention—preventive strategies to reduce the risk factors for ischemic stroke, such as carotid artery stenosis, have extensively gained attention from researchers [ 6 ]. The knowledge accrued from the utilization of preclinical models of cerebral hypoperfusion/revascularization injury [ 5 ] has allowed not only to identify the nature and dynamics of the reperfusion injury [ 1 , 6 , 7 , 8 ] but also to correlate hypoperfusion/reperfusion to reliable biomarker changes. So far, evidence in this area of research shows that the acute transient bilateral common carotid artery occlusion followed by reperfusion (BCCAO/R) is a model that can mimic in vivo the biological effects of acute cerebral oxidative stress and the early formation of a deleterious pro-inflammatory milieu [ 9 , 10 ].…”

Changes in the cerebral cortex and thyroid in the simulation of cerebral hypoperfusion and its combination with physical exercise

“…2-я группа -модель церебральной гипоперфузии (ЦГ) -двусторонняя перевязка общих сонных артерий под общей анестезией золетилом. Данная методика является «золотым стандартом» долговременной церебральной гипоперфузии у животных [4]. 3-я группа -экспериментальная (ЦГ + СП), ее составили животные с моделью церебральной гипоперфузии, которым начиная с 8-го дня после операции и на протяжении дальнейшего исследования, максимум на протяжении 28 дней (до 35 сут.…”

“…Подавляющее число хронических заболеваний головного мозга тесно связано со снижением гемоперфузии, которая запускает ряд клеточных механизмов: нейродегенерацию [1], некроз и апоптоз нейронов [2], активацию и гибель астроцитов [3] и олигодендроглиоцитов, микроглиальную и астроглиальную активацию, повреждение гемато-энцефалического барьера [4], нарушение гемореологии и гемомикроциркуляции, эндотелиальную дисфункцию, окислительный стресс [5], нейровоспаление, приводящее к снижению когнитивных способностей [6]. Исследования В.Н.…”