Introduction Cerebral ischemia, also known as ischemic stroke, occurs when there is insufficient blood flow to the brain, resulting in the deprivation of oxygen and nutrients necessary for brain cell survival. This condition can lead to significant brain damage and various neurological deficits. The pathogenesis of cerebral infarction is caused by atherosclerosis, thrombosis, embolism, hemorheological, hemostatic fibrinolysis, as well as heart diseases (heart attack, arrhythmia, congenital and acquired valvular abnormalities), C and S protein deficiency, homocystinuria, polycythemia, and other factors. Stroke is the most common cause of disability and the fourth most common cause of death in the developed world. The great majority of strokes can be prevented through blood pressure control, and the ideal treatment is to improve cerebral blood supply and cerebral blood flow.
Understanding cerebral ischemia is crucial for developing effective treatments and preventive strategies. In-vivo models of ischemic stroke have been developed, which allow us to explicate the pathophysiological mechanisms of injury further and investigate potential drug targets. These models directly replicate the reduction in blood flow and the resulting impact on nervous tissue. The most frequently used in vivo model of ischemic stroke is the intraluminal suture middle cerebral artery occlusion (iMCAO, BCCAO) model, which has been fundamental in revealing various aspects of stroke pathology.
This review study conducted to establish a pathologically relevant model of cerebral ischemia in experimental animals, further investigate the therapeutic effect, and develop new medicines.