de la Torre J C, Fortin T
Division of Neurosurgery, University of Ottawa Health Sciences, Ontario.
Brain Res Bull. 1991 Mar;26(3):365-72. doi: 10.1016/0361-9230(91)90008-8.
A model for inducing partial (PBI) or global brain ischemia (GBI) in awake or anesthetized rats was obtained by ligating one subclavian and both carotid arteries (for PBI) or both subclavian-carotid arteries (for GBI). Rats were intubated and ventilated mechanically then subjected to a midline ventral incision from larynx to xiphoid process. The thorax was entered to expose the aortic arch and either one or both subclavians were ligated to eliminate each vertebral artery supply to brain. After chest closure the common carotid arteries were exposed and immediately ligated or else catheter snares were installed to induce ischemia at a later date. PBI was induced in 3 groups of rats for 7, 30 and 60 days while GBI was given for 5, 10, 30 and 75 minutes in 4 other groups. EEG became flat within 15 seconds after GBI and cortical cerebral blood flow (CBF) was reduced to "zero." EEG was unaffected after PBI but cortical CBF was reduced from a mean 118 ml/100 g tissue/min to 77 ml after 7 days. Morphological damage of CA1 hippocampal neurons after GBI or PBI was found reproducible and time dependent on ischemic duration. Acute cell damage rose from 5-95% in CA1 as GBI duration increased from 5-75 minutes. Similarly, chronic cell damage of CA1 increased as ischemic duration continued from 7-60 days in rats subjected to PBI. The advantages of the present model provide the option of inducing partial or global brain ischemia and of introducing postischemic reperfusion in awake or anesthetized preparations without the use of drugs, blood pressure manipulation or direct contact with brain tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
通过结扎一侧锁骨下动脉和双侧颈动脉（用于部分脑缺血，PBI）或双侧锁骨下 - 颈动脉（用于全脑缺血，GBI），建立了在清醒或麻醉大鼠中诱导部分或全脑缺血的模型。大鼠经气管插管并机械通气，然后从喉部至剑突进行中线腹侧切口。打开胸腔暴露主动脉弓，结扎一侧或双侧锁骨下动脉以消除每条椎动脉对脑的供血。关闭胸腔后，暴露双侧颈总动脉并立即结扎，或者安装导管圈套器以便日后诱导缺血。3组大鼠接受PBI诱导7、30和60天，另外4组大鼠接受GBI诱导5、10、30和75分钟。GBI后15秒内脑电图变平，皮质脑血流量（CBF）降至“零”。PBI后脑电图未受影响，但7天后皮质CBF从平均118 ml/100 g组织/分钟降至77 ml。发现GBI或PBI后海马CA1神经元的形态学损伤具有可重复性，且与缺血持续时间呈时间依赖性。随着GBI持续时间从5分钟增加到75分钟，CA1区急性细胞损伤从5%上升至95%。同样，在接受PBI的大鼠中，随着缺血持续时间从7天延长至60天，CA1区慢性细胞损伤增加。本模型的优点是可以选择在清醒或麻醉状态下诱导部分或全脑缺血，并在不使用药物、不操纵血压或不直接接触脑组织的情况下引入缺血后再灌注。（摘要截断于250字）
