Effect of the 21-aminosteroid U-74006F on cerebral vasospasm following subarachnoid hemorrhage.
Effect of the 21-aminosteroid U-74006F on cerebral vasospasm following subarachnoid hemorrhage.
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21-氨基类固醇 U-74006F 对蛛网膜下腔出血后脑血管痉挛的影响。
DOI：
10.3171/jns.1989.71.1.0098
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发表时间：
1989
影响因子：
4.1
通讯作者：
D. K. Anderson
中科院分区：
文献类型：
--
作者：
M. Zuccarello;Jeffery T. Marsch;Gerald Schmitt;James Woodward;D. K. Anderson
本研究的目的是使用一种新的21-氨基类固醇（U-74006 F），在体外抗氧化和抗脂肪分解特性作为药理学探针，以评估在兔模型的蛛网膜下腔出血（SAH）引起的血管痉挛的脂质水解和过氧化作用。对15只家兔进行脑血管造影。18小时后，将1 cc/kg自体血液输注到所有15只动物的小脑延髓池中。六只兔子不接受治疗，六只在SAH后30分钟开始接受U-74006 F，三只兔子在SAH后30分钟开始接受U-74006 F的媒介物。在SAH后72小时，获得第二次血管造影。数字减影血管造影技术用于测量基底动脉的直径和造影剂流量。在SAH后72小时，所有未处理和溶剂处理的兔中血管痉挛明显。基底动脉的直径和通过基底动脉的流量分别显著降低42.3% +/- 6.6%和46.8% +/-5.8%，低于SAH前水平（平均值+/-平均值的标准误差）。用U-74006 F治疗消除了SAH诱导的血管痉挛;在治疗的动物中，基底动脉的流量和直径均处于SAH前水平。这些调查结果表明：1）膜脂质变化（即，类二十烷酸水解和/或过氧化）导致SAH引起的慢性血管痉挛，2）U-74006 F通过限制这些病理性膜事件预防该模型中SAH诱导的慢性血管痉挛。
The purpose of this study was to use a new 21-aminosteroid (U-74006F) with in vitro antioxidant and antilipolytic properties as a pharmacological probe to assess the role of lipid hydrolysis and peroxidation in a rabbit model of subarachnoid hemorrhage (SAH)-induced vasospasm. Cerebral angiograms were performed on 15 rabbits. Eighteen hours later, 1 cc/kg of autologous blood was infused into the cisterna magna of all 15 animals. Six rabbits received no treatment, six received U-74006F starting 30 minutes after SAH, and three rabbits received the vehicle for U-74006F starting 30 minutes after SAH. At 72 hours post-SAH, a second angiogram was obtained. Digital subtraction angiographic techniques were used to measure the diameter of and contrast material flow through the basilar artery. At 72 hours post-SAH, vasospasm was evident in all untreated and vehicle-treated rabbits. The diameter of and the flow through the basilar artery were significantly reduced 42.3% +/- 6.6% and 46.8% +/- 5.8%, respectively, below pre-SAH levels (means +/- standard error of the means). Treatment with U-74006F eliminated the SAH-induced vasospasm; in treated animals, both the flow through and the diameter of the basilar arteries were at pre-SAH levels. These findings indicate that: 1) membrane lipid changes (that is, hydrolysis with eicosanoid production and/or peroxidation) contribute to the chronic vasospasm resulting from SAH, and 2) U-74006F prevents the SAH-induced chronic vasospasm in this model by limiting these pathological membrane events.
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