| 摘要: |
| 目的 探讨兔颈动脉外膜损伤后血管粥样硬化(AS)程度与动脉内去甲肾上腺素含量及交感神经密度的关系，并分析通心络对AS的作用效果及可能机制。方法 采用Ⅰ型胶原酶局部损伤兔颈动脉外膜结合高脂喂养的方法，制备颈动脉外膜损伤致动脉粥样硬化模型，将模型动物随机分为2组:外膜损伤组、通心络治疗组；组内对左侧颈动脉行外膜损伤，右侧作为自身对照。分别于术后1、3、7 d、2、4、8周取血及双侧颈动脉，采用酶联免疫吸附法(ELISA)检测兔血清及动脉壁中去甲肾上腺素含量，免疫组化法检测血管外膜交感神经密度。结果 外膜损伤组左侧颈动脉内膜增生面积明显大于右侧，内膜增生面积与神经染色强度及局部动脉壁去甲肾上腺素含量呈正相关(r=0.94,P<0.05;r=0.90,P<0.05)；与外膜损伤组相比，通心络能够明显减轻外膜损伤后血管内粥样斑块面积\[IMR(48±2)% vs (70±3)%,P<0.01\]，降低动脉壁组织中去甲肾上腺素含量\[(83.76±3.3) ng/g vs (74.25±2.1) ng/g,P<0.05\]及血管的交感神经密度(P<0.05)。结论 外膜损伤可加重高脂饮食诱导的AS病变程度，部分可能与其促进局部交感神经功能失调有关，通心络能够拮抗外膜损伤诱导的AS病变。 |
| 关键词: 动脉粥样硬化 交感神经系统 去甲肾上腺素 颈动脉 外膜损伤 通心络 |
| DOI：10.3724/SP.J.1008.2010.0585 |
| 投稿时间：2009-06-16修订日期：2010-04-26 |
| 基金项目:国家重点基础研究发展计划(“973”计划，2005CB523309). |
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| Influence of adventitia injury-induced atherosclerosis on sympathetic nerve function in rabbits |
| CHEN Wei, LIANG Chun, LIU Xing, WANG Hua, ZHOU Wei-jian, WU Zong-gui* |
| (Department of Cardiology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China) |
| Abstract: |
| Objective To evaluate the effect of adventitia injury on atherosclerosis(AS)development, norepinephrine content, and sympathetic nerve density in the carotid artery of rabbits, so as to analyze the effect of Tongxinluo(TXL) on AS and the possible mechanism. Methods Totally 96 male rabbits with left carotid adventitia removed were fed with high cholesterol diet and were divided into two groups randomly:one group was lavaged with TXL (TXL group) and the other with water (adventitia injury group). In each group the adventitia of left cervical artery was injured and the right one served as control. The bilateral carotid artery specimens and blood samples were collected 1 d, 3 d, 7 d, 2 w, 4 w, and 8 w after the operation．The norepinephrine contents in serum and carotid artery were determined by ELISA and the density of the sympathetic nerve was analyzed by immnohistochemical method. Results In the adventitia injury group adventitia injury aggravated AS in the left carotid artery compared with that in the right carotid artery; the area of atherosclerotic plaque was positively correlated with the nerve density(r=0.94，P<0.05)and local norepinephrine content in the artery (r=0.90，P<0.05). TXL significantly decreased the area of atherosclerotic plaque compared to the advetitia injury group (IMR\[48±2\]% vs \[70±3\]%,P<0.01); besides, it also decreased the level of norepinephrine in the artery(\[83.76±3.3\] ng/g vs \[74.25±2.1\] ng/g, P<0.05)and the density of the sympathetic nerve(P<0.05). Conclusion Adventitia injury can promote the development of AS in high-cholesterol fed animals, partially through promoting the disorder of local sympathetic function, and TXL can inhibit the adventitia injury-induced AS. |
| Key words: atherosclerosis sympathetic nervous system norepinephrine carotid artery adventitia injuries Tongxinluo |
