1. Animal modeling materials: Male SD rats, weighing 280-350g; Medication: Chloral hydrate, antibiotics.
2. Method of modeling: Anesthesia was injected intraperitoneally with 10% chloral hydrate (300mg/kg), fixed in an upward position on a rat plate, and a skin incision of about 2cm was made along the middle of the neck. The right common carotid artery was separated and two sutures were threaded for backup. The external carotid artery was then separated and ligated. Carefully separate the internal carotid artery and its adjacent small branch (pterygopalatine artery) below the external carotid artery, thread a suture under the branch, and ligate it near the bifurcation. The proximal end of the separated common carotid artery is blocked with an arterial clamp, while the distal end is gently pulled up with a suture. A small incision is made on the common carotid artery, and a nylon rod heated to a ball shape (0.28mm) at one end is inserted into the small opening. Slowly push it into the anterior cerebral artery (about 20mm), and then pull it back about 2mm to reach the middle cerebral artery opening, which is about 17mm long (calculated from the bifurcation of the internal and external carotid arteries). The nylon rod is ligated and fixed with suture. Ligate the proximal end with another suture, remove the arterial clamp, suture the muscles and skin, and return to the cage for feeding after the surgery is completed. The sham operated group rats were only exposed to the common carotid artery, external carotid artery, and internal carotid artery without ligation.
3. Modeling principle: Ligation of blood vessels leads to cerebral ischemia.
4. Changes after modeling: The neurological function score of the model group rats was 2.3 ± 0.8, the infarct area was (21.6 ± 6.7)%, and the brain water content was (81.1 ± 1.3)%. The water content of the brain tissue in the sham operated group was (78.5 ± 0.7)%.