Meng W, Busija D W
Department of Physiology and Pharmacology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina, USA.
J Cereb Blood Flow Metab. 1996 Jan;16(1):175-9. doi: 10.1097/00004647-199601000-00021.
This study examined the role of oxygen radicals in pial arteriolar changes during cortical spreading depression (CSD). CSD was induced by microinjection of 5% KCl in anesthetized adult rabbits. Pial diameter was measured with a closed cranial window and intravital microscopy. During control CSD (n = 12), the dilation amplitude and area were 55 +/- 14% and 693 +/- 69 mm2 (baseline = 76 +/- 14 microns), respectively. Oxygen radical scavengers, superoxide dismutase (SOD; 105 U/ml, topical application; n = 5) or oxypurinol (50 mg/kg i.v.; n = 7), did not alter the dilation amplitude and area or change onset latency during CSD. Further, SOD and oxypurinol did not prevent NG-nitro-L-arginine from attenuating arteriolar dilation during CSD (n = 12). We conclude that oxygen radicals do not play a role in the transient dilation of cerebral arterioles during CSD.
本研究探讨了氧自由基在皮层扩散性抑制（CSD）期间软脑膜小动脉变化中的作用。通过向麻醉的成年兔脑内微量注射5%氯化钾诱导CSD。使用封闭颅窗和活体显微镜测量软脑膜直径。在对照CSD（n = 12）期间，扩张幅度和面积分别为55±14%和693±69 mm2（基线 = 76±14微米）。氧自由基清除剂超氧化物歧化酶（SOD；105 U/ml，局部应用；n = 5）或氧嘌呤醇（50 mg/kg静脉注射；n = 7），在CSD期间并未改变扩张幅度和面积，也未改变起始潜伏期。此外，SOD和氧嘌呤醇不能阻止NG-硝基-L-精氨酸在CSD期间减弱小动脉扩张（n = 12）。我们得出结论，氧自由基在CSD期间脑小动脉的短暂扩张中不起作用。
