Miyashita K, Abe H, Nakajima T, Ishikawa A, Nishiura M, Sawada T, Naritomi H
Department of Medicine, National Cardiovascular Centre, Osaka, Japan.
Neuroreport. 1994 Dec 30;6(1):46-8. doi: 10.1097/00001756-199412300-00013.
We investigated the induction of ischaemic tolerance in the hippocampal CA1 neurones to transient forebrain ischaemia following pretreatment with unilateral middle cerebral artery occlusion (MCAO) in gerbils. Histological evaluation was carried out after 5 min bilateral carotid artery occlusion (5BCO) in the gerbils with no MCAO pretreatment, MCAO pretreatment 3 days prior to 5BCO (MCAO-3d-5BCO), MCAO pretreatment 7 days prior to 5BCO and sham MCAO pretreatment 3 days prior to 5BCO. CA1 neurones were preserved at > 40% of normal controls only in the left hippocampus in the MCAO-3d-5BCO gerbils. CA1 neurones in the right side of MCAO-3d-5BCO gerbils as well as in both sides of animals in the other pretreatment groups almost completely disappeared after 5BCO. While the exact mechanism remains to be resolved, pretreatment with focal ischaemia seems to induce ischaemic tolerance in neurones outside of the primary ischaemic lesion.
我们研究了沙土鼠经单侧大脑中动脉闭塞（MCAO）预处理后，海马CA1神经元对短暂性全脑缺血的缺血耐受诱导情况。对未进行MCAO预处理的沙土鼠、在5分钟双侧颈动脉闭塞（5BCO）前3天进行MCAO预处理的沙土鼠（MCAO-3d-5BCO）、在5BCO前7天进行MCAO预处理的沙土鼠以及在5BCO前3天进行假MCAO预处理的沙土鼠，在5分钟双侧颈动脉闭塞后进行了组织学评估。仅在MCAO-3d-5BCO沙土鼠的左侧海马中，CA1神经元的保留率大于正常对照组的40%。在5BCO后，MCAO-3d-5BCO沙土鼠右侧的CA1神经元以及其他预处理组动物双侧的CA1神经元几乎完全消失。虽然确切机制仍有待解决，但局灶性缺血预处理似乎能在原发性缺血损伤以外的神经元中诱导缺血耐受。
