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在皮质扩散性抑制期间,氧自由基在小动脉扩张过程中不起作用。

Oxygen radicals do not play a role in arteriolar dilation during cortical spreading depression.

作者信息

Meng W, Busija D W

机构信息

Department of Physiology and Pharmacology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina, USA.

出版信息

J Cereb Blood Flow Metab. 1996 Jan;16(1):175-9. doi: 10.1097/00004647-199601000-00021.

Abstract

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.

摘要

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。

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