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作 者:王双全[1] 段传志[1] 姜晓丹[1] 姬斌[1] 杜谋选[1] 薛杉[1] 张鹏[1] 法志强[1] 王建奇[1]
机构地区:[1]南方医科大学广东神经外科研究所,南方医科大学珠江医院神经外科,广东省脑功能修复与再生重点实验室,广州510282
出 处:《中华神经医学杂志》2009年第12期1217-1220,共4页Chinese Journal of Neuromedicine
基 金:国家“十一五”科技支撑项目分课题(2006BAI01A12);广东省科技计划项目(2006836001006);广东省自然科学基金(8251051501000012);南方医科大学中青年优秀科技人才资源项目
摘 要:目的建立雌激素缺乏的颅内动脉瘤模型,并在此基础上初步研究雌激素缺乏对颅内动脉瘤形成、生长的影响及其可能机制。方法雌性Wistar大鼠30只按随机数字表法分为实验组(切除双侧卵巢+颅内动脉瘤模型)、实验对照组(切除双侧卵巢旁与其大小相当的一块脂肪+颅内动脉瘤模型)、空白对照组(每组各10只)。大鼠去势模型或腹部假手术模型制作后2周用猪胰弹性蛋白酶滴加到颈外动脉及分叉处动脉壁周围,在颈外动脉距分叉处约1.5mm位点用两根手术线结扎颈外动脉,在两根线之间剪断颈外动脉,使颈外动脉的盲段形成颈内动脉的一个动脉瘤。动脉瘤模型制作6周后取右心房全血2mL,离心取上清液后于-20℃冰箱保存,用于检测大鼠血清中雌激素的含量,同时游标卡尺测量颅内动脉瘤长度和直径,并取实验组及实验对照组的颅内动脉瘤组织和空白对照组相应的一段颈外动脉组织用于常规组织切片染色。结果实验组血清中雌激素水平为(105.00±12.96)pmol/L,实验对照组为(178.50±25.96)pmol/L,空白对照组为(180.40±18.70)pmol/L,实验组与实验对照组及空白对照组组间比较差异有统计学意义(P〈0.05)。实验组颅内动脉瘤长度扩张率为(131.31±6.63)%,直径扩张率为(125.10±5.49)%,实验对照组为(109.90±3.44)%和(106.82±2.49)%,比较差异有统计学意义(P〈0.05)。结论雌激素缺乏对颅内动脉瘤的形成、生长有一定的促进作用。本研究使用盲段法结合酶消化法制作颅内动脉瘤模型简便可行。Objective To construct an aneurismal model with estrogen deficiency and investigate the mechanism of estrogen deficiency in the formation and development of intracranial aneurysm. Methods Female Wistar rats were randomly divided into experimental, sham-operative and blank control groups (n=10). Rats in the experimental group were ovariectomized and those in the sham-operative group were removed the adipose issue nearby the ovary only; while the rats in the blank control group were done nothing. Two weeks after the ovariectomized or sham operation, elastase dropped around the fight external carotid artery and the crotch of the carotid artery and the carotid artery was ligated by two lines at 1.5 mm far from the crotch, and then sheared between the two lines to successfully induce the aneurysm. At 6 weeks of the successful construction of aneurysm model, the estrogen was detected and the aneurysm was harvested for pathological staining. Results The experimental group showed a lower estrogen level (105.00±12.96 pmol/L) than the sham-operative group (178.50±25.96 pmol/L) and the blank control group (180.40±18.70 pmol/L, P〈0.05). Aneurismal length dilatation rates in the experimental group and the sham-operative group were (131.31 ±6.63) % and (109.90±3.44) %, respectively (P〈0.05). Aneurismal diameter dilatation rates in the experimental group and sham-operative group were (125.10±5.49) % and (106.82±2.49) %, respectively (P〈0.05). Conclusion Estrogen deficiency may promote the formation and development of the intracranial aneurysm. This experiment provides a simple model for investigating the relationship between estrogen deficiency and aneurysm development.
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