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Bihemispheric ischemic tolerance induced by a unilateral focal cortical lesion

机译：单侧局灶性皮层病变诱发的双半球缺血耐受

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摘要

The purpose of the present study was to determine whether a unilateral photothrombotic brain lesion induces bilateral ischemic tolerance towards a subsequent severe ischemia performed 5 days later. Severe ischemia was induced by transient (1 h; t) or permanent (p) occlusion of the middle cerebral artery (MCAO). Rats were sacrificed 24 h later. Preconditioning reduced the size of subsequent infarcts in both hemispheres. This effect was most prominent with tMCAO, and ipsilateral preconditioning was more effective than contralateral preconditioning (% of hemispheric volume, mean + SD: 31.9 + 3.7 to 19.0 + 10.3 with ipsilateral tMCAO; 31.9 + 3.7 to 22.9 + 4.9 with contralateral tMCAO; 64.7+4.3% to 47.2 + 12.5% with ipsilateral pMCAO; 64.7+4.3% to 53.1 + 8.9% with contralateral pMCAO). Ischemic preconditioning was associated with a successive bilateral up-regulation of superoxide dismutases which may be involved in the development of ischemic tolerance. Our data suggest that a focal ischemic brain lesion induces neuroprotective mechanisms in extensive brain areas and thus cause bilateral ischemic tolerance within a certain time window.
机译：本研究的目的是确定单侧光血栓性脑损伤是否对5天后进行的随后的严重缺血诱导双侧缺血耐受。大脑中动脉短暂（1 h; t）或永久（p）闭塞（MCAO）引起严重缺血。 24小时后处死大鼠。预处理可减少两个半球随后的梗塞面积。使用tMCAO时效果最明显，同侧预处理比对侧预处理更有效（同侧tMCAO占半球体积的百分比，平均值+ SD：31.9 + 3.7至19.0 + 10.3;对侧tMCAO占31.9 + 3.7至22.9 + 4.9; 64.7同侧pMCAO为+ 4.3％至47.2 + 12.5％;对侧pMCAO为64.7 + 4.3％至53.1 + 8.9％）。缺血预处理与超氧化物歧化酶连续的双边上调相关，超氧化物歧化酶可能参与缺血耐受的发展。我们的数据表明局灶性缺血性脑损伤在广泛的脑区域诱导神经保护机制，从而在一定时间范围内引起双侧缺血耐受。

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