山莨菪碱对蛛网膜下腔出血后基底动脉产生EDRF的作用及抗痉挛机制研究

Effect of anisodamine on production of endothelium derived relaxing factor following subarachnoid hem orrhage in rabbit basilar artery and its anti-vasospasm mechanism

用山莨菪碱（６５４－２）防治蛛网膜下腔出血（ＳＡＨ）后脑血管痉挛，观察６５４－２对基底动脉中ＥＤＲＦ，ＭＤＡ，ＳＯＤ，ｃＧＭＰ，Ｃａ￣（２＋），Ｎａ￣＋的影响。结果表明，应用６５４－２后降低了基底动脉中ＭＤＡ产生及Ｃａ￣（２＋）Ｎａ￣＋的含量，与ＳＡＨ组比，ＥＤＲＦ释放增加，ＳＯＤ活性及ｃＧＭＰ水平提高，基底动脉内皮细胞受到保护，基底动脉收缩幅度减小。提示，６５４－２可通过保护内皮细胞，减轻氧自由基损伤，拮抗Ｃａ￣（２＋）Ｎａ￣＋在细胞内的蓄积，从而促进内皮细胞ＥＤＲＦ释放，引起血管舒张，明显减轻ＳＡＨ后的脑血管痉挛。

Anisodamine(654-2)was used to prevent the cerebral vasospasm fol-lowing subarachnoid hemorrhage(SAH ), and the effect of 654-2 on endothelium deriv-ed relaxing factor(EDRP) , malondiadehyde(MDA),superoxide dismutase( SOcGMP,Ca￣(2+) and Na￣+ in the basilar arteries were observed. Results showed that compar-ed with SAH group, while the rabbits were treated with 654-2 before and after SAH,the contents of MDA, Ca￣(2+) and Na￣+ decreased and release of EDRF increased in the basilar arteries. 654-2 also enhanced SOD activity and cGMP level of the basilar arteries. In turn it attenuated the endothelial cells injury and vasospasm of the basilararteries respectively. These results suggested that 654-2 may promcte the releaseof EDRF from endothelial cells by attenuate the injury of basilar arteries which wasinduced by free radicals and reduced Ca￣(2+) and Na￣+ accumulation in cells and finallypreventedthe cerebral vascspasm following SAH.