Zwagerman Nathan, Sprague Shane, Davis Michael Duff, Daniels Bradley, Goel Gunjan, Ding Yuchuan
Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, USA.
Neurol Res. 2010 Jun;32(5):523-9. doi: 10.1179/016164109X12581096796431. Epub 2010 Jan 21.
The neuroprotective nature of exercise has been well established and the mechanisms of this protection are still a subject of much research. This study aims to determine if cerebral blood flow is constituently higher during the ischemia or reperfusion events in stroke.
Adult male Sprague-Dawley rats were randomly assigned into exercise or non-exercise (control) groups. Exercised rats underwent 30 minutes of running on a treadmill for 3 weeks. A 2 hour unilateral middle cerebral artery occlusion using an intraluminal filament was performed to induce ischemic stroke, followed by a 24 hour reperfusion. A sham control without exercise and middle cerebral artery occlusion was used. Laser Doppler flowmetry (LDF) and (15)O-H(2)O positron emission tomography (PET) were used to determine cerebral blood flow, respectively. (18)F-fluorodeoxy-D-glucose was used to determine cerebral metabolism in some animals. Histological analysis determined infarct volume in the same animal after blood flow examination.
LDF and PET both indicated that middle cerebral artery occlusion significantly (p<0.05) reduced cerebral blood flow during ischemia and reperfusion in association with reduced cerebral metabolism after stroke. However, pre-ischemic exercise significantly (p<0.05) improved cerebral blood flow during reperfusion, although cerebral blood flow remained at a similar level to that of the non-exercise stroke group during the middle cerebral artery occlusion. This improved cerebral blood flow during reperfusion was associated with decreased brain infarct volume.
This study revealed that pre-ischemic exercise in rats improved cerebral blood flow during reperfusion, suggesting that exercise provides neuroprotection by partially ameliorating the 'no reflow' phenomenon in stroke.
运动的神经保护特性已得到充分证实,但其保护机制仍是众多研究的主题。本研究旨在确定在中风的缺血或再灌注事件期间脑血流量是否持续更高。
成年雄性Sprague-Dawley大鼠被随机分为运动组或非运动(对照)组。运动组大鼠在跑步机上跑步30分钟,持续3周。使用腔内细丝进行2小时的单侧大脑中动脉闭塞以诱导缺血性中风,随后进行24小时再灌注。使用未运动且未进行大脑中动脉闭塞的假手术对照组。分别使用激光多普勒血流仪(LDF)和(15)O-H2O正电子发射断层扫描(PET)来测定脑血流量。在一些动物中使用(18)F-氟脱氧-D-葡萄糖来测定脑代谢。组织学分析在血流检查后确定同一动物的梗死体积。
LDF和PET均表明,大脑中动脉闭塞在缺血和再灌注期间显著(p<0.05)降低了脑血流量,同时中风后脑代谢降低。然而,缺血前运动在再灌注期间显著(p<0.05)改善了脑血流量,尽管在大脑中动脉闭塞期间脑血流量与非运动中风组保持在相似水平。再灌注期间这种改善的脑血流量与脑梗死体积减小有关。
本研究表明,大鼠缺血前运动改善了再灌注期间的脑血流量,提示运动通过部分改善中风中的“无复流”现象提供神经保护。