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组氨酸可减轻兔蛛网膜下腔出血模型中的脑血管痉挛。

Histidine attenuates cerebral vasospasm in a rabbit model of subarachnoid hemorrhage.

作者信息

Fadel M M, Foley P L, Kassell N F, Lee K S

机构信息

Department of Neurological Surgery, University of Virginia, Charlottesville 22908, USA.

出版信息

Surg Neurol. 1995 Jan;43(1):52-7; discussion 57-8. doi: 10.1016/0090-3019(95)80038-i.

DOI:10.1016/0090-3019(95)80038-i
PMID:7701424
Abstract

BACKGROUND

Free radical generation following hemolysis of a subarachnoid blood clot is believed to be a key component in the development of cerebral vasospasm. Histidine, an essential amino acid with free radical scavenging characteristics, was examined for its effects on cerebral vasospasm.

METHODS

An experimental rabbit model of subarachnoid hemorrhage-induced vasospasm was used in which autologous arterial blood was injected into the cisterna magna. Basilar arteries were removed following perfusion-fixation two days after the injection of blood, and their cross-sectional luminal areas were measured using computerized image analysis. Rabbits received intravenous injections of L-histidine or vehicle starting 30 min prior to induction of subarachnoid hemorrhage (SAH), with additional injections given four times per day for the next 2 days.

RESULTS

The luminal area of arteries from animals treated with histidine (50 mg/kg/dose or 100 mg/kg/dose) were significantly larger than those from vehicle-treated animals. Relative to the SAH-only groups (mean cross-sectional area = 106.8 x 10(3) microns 2), vasoconstriction was attenuated by 31% in the low dose treatment group (180.0 x 10(3) microns 2) and by 52% in the high dose treatment group (227.4 x 10(3) microns 2). Mean luminal area of control basilar arteries was 340.5 x 10(3) microns 2.

CONCLUSIONS

These findings demonstrate that histidine reduces the amount of cerebral vasospasm occurring subsequent to experimental SAH. It is suggested that the free radical scavenging characteristics of histidine, particularly its ability to scavenge singlet oxygen, may be responsible for the reduction in vasospasm.

摘要

背景

蛛网膜下腔血凝块溶血后自由基的产生被认为是脑血管痉挛发生过程中的一个关键因素。组氨酸是一种具有自由基清除特性的必需氨基酸,本研究对其对脑血管痉挛的影响进行了检测。

方法

采用实验性兔蛛网膜下腔出血诱导血管痉挛模型,将自体动脉血注入枕大池。在注入血液两天后进行灌注固定,然后取出基底动脉,使用计算机图像分析测量其横断面管腔面积。兔在蛛网膜下腔出血(SAH)诱导前30分钟开始静脉注射L-组氨酸或赋形剂,并在接下来的2天内每天额外注射4次。

结果

用组氨酸(50mg/kg/剂量或100mg/kg/剂量)治疗的动物的动脉管腔面积显著大于用赋形剂治疗的动物。相对于仅SAH组(平均横截面积=106.8×10³微米²),低剂量治疗组(180.0×10³微米²)的血管收缩减弱了31%,高剂量治疗组(227.4×10³微米²)的血管收缩减弱了52%。对照基底动脉的平均管腔面积为340.5×10³微米²。

结论

这些发现表明,组氨酸可减少实验性SAH后发生的脑血管痉挛量。提示组氨酸的自由基清除特性,特别是其清除单线态氧的能力,可能是血管痉挛减轻的原因。

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