Tokunaga H, Hiramatsu K, Sakaki T
Department of Neurosurgery. Nara Medical University, 840 Shijyou-cho, Kashihara, Nara 634, Japan.
Brain Res. 1998 Feb 16;784(1-2):316-20. doi: 10.1016/s0006-8993(97)01237-7.
We investigated the mechanism of 'ischemic tolerance phenomenon' by characterizing the physiological events, modified by preceding sublethal ischemia, during secondary hypoxia. Slices from brains after pretreatment of sublethal forebrain ischemia were subjected to a 70% reduction of PO2 (threshold hypoxia). Although evoked potentials disappeared completely in five of eight slices from sham-operated brain, they were sustained in 28/32 slices from pretreated brains. This study indicates that the maintenance of membrane function might be the mechanism of ischemic tolerance.
我们通过描述在继发性缺氧期间由先前的亚致死性缺血所改变的生理事件,来研究“缺血耐受现象”的机制。对经亚致死性前脑缺血预处理后的大脑切片进行70%的氧分压降低(阈值缺氧)处理。虽然假手术组大脑的8个切片中有5个切片的诱发电位完全消失,但预处理组大脑的32个切片中有28个切片的诱发电位得以维持。本研究表明,膜功能的维持可能是缺血耐受的机制。