摘要
目的 观察局灶性缺血预处理所诱导的脑缺血耐受现象及其存在的时间窗。方法 86只 SD大鼠随机分为 PC、PC+ MCAO及 SS+ MCAO三组 ,分别给予 10 min大脑中动脉缺血预处理 ( PC)、PC+ 2 h大脑中动脉阻塞 ( MCAO)及假手术 ( SS) + 2 h MCAO,其中后两组又据 PC与 MCAO间隔不同分为 1d,3 d,7d,14d,2 1d,2 8d 6个亚组 ,MCAO后 2 4h处死 ,比较各组神经功能评分、梗死体积、含水量及组织病理变化。结果 单纯 PC不引起神经功能缺损及梗死形成 ;MCAO前 1～ 2 8d给予 PC组神经功能缺损均轻于 SS组 ( P<0 .0 1) ,其中 3 d组最明显 ;MCAO前 1～ 14d给予 PC者较 SS组梗死体积缩小 ( P<0 .0 5 ) ,尤以 3 d及 7d组明显 ,分别减小 5 3 .7%和49.9% ( P<0 .0 1) ;MCAO前 3 d给予 PC组脑含水量低于 SS组 ( P<0 .0 5 )。结论 10 min大脑中动脉预缺血不会引起神经损害但已足以诱导缺血耐受的产生 ;缺血耐受作用出现于 PC后 1d,其后 14d内给予 MCAO均可使梗死体积减小 ,而对神经功能的保护作用持续时间更长 ,至少可达
Objective To investigate the ischemic tolerance induced by focal ischemic preconditioning (PC) in rats. Methods Ten minutes of middle cerebral artery occlusion(MCAO) was used for PC. Different duration of reperfusion (1,3,7,14,21 and 28 days) was allowed before 2 hours of MCAO followed by 22 hours of reperfusion in SD rats that were divided into the PC group and the PC plus MCAO group, and were compared with the rats of sham-operation plus MCAO group. Neurological scores, infarct volume, brain water content and HE staining were evaluated in each group. Results PC produced no neurological deficits and TTC-demonstrated infarct. PC reduced neurological deficits significantly caused by 2h MCAO 1-28 days after PC. Infarct volume was reduced only if PC was performed 1-14 days before MCAO. PC given 3 days before MCAO also decreased brain water content. Conclusion Ten minutes of MCAO was strong enough to induce ischemic tolerance without brain injury. Infarct volume reduction appeared at 1 day and did not vanish until 14 days after PC, but protection against neurological impairment existed at least 4 weeks.
出处
《四川大学学报（医学版）》
CAS
CSCD
北大核心
2003年第3期455-458,共4页
Journal of Sichuan University(Medical Sciences)
