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作 者:缪朝玉[1] 陶霞[1] 管云枫[1] 杨友才[1] 楚正绪[1] 苏定冯[1]
机构地区:[1]第二军医大学基础医学部药理学教研室,上海200433
出 处:《第二军医大学学报》2000年第8期734-738,共5页Academic Journal of Second Military Medical University
基 金:国家自然科学基金!资助项目 (396 70 831)
摘 要:目的 :观察去窦弓神经 (SAD)大鼠主动脉重建及发生发展过程 ,初步探讨体液因素在其中的作用。 方法 :计算机图像分析测定主动脉形态 ;离体血管制备观察主动脉功能 ;放免法测定 Ang 浓度。 结果和结论:(1)主动脉结构重建在 SAD后 4~ 16周时随时间延长而加重。从几何形态学和中膜显微结构改变来看 ,主动脉结构重建主要属血管肥厚型 ,且与平滑肌生长和胶原积聚有关。 (2 )主动脉对 NE的收缩反应在 SAD后 8~ 32周时进行性增强 ,对 ACh的舒张反应在 SAD后 8~ 32周时减弱。 SAD后 32周时主动脉去内皮后对 NE的收缩反应增强作用消失。提示血管功能改变与内皮和 (或 )内皮与平滑肌的相互作用改变有关。 (3) SAD后 10周时 ,血浆 Ang 浓度无明显改变 ,而主动脉 Ang 浓度升高。提示组织 RAS激活可能参与Objective: To study aortic remodeling produced by chronic sinoaortic denervation (SAD) and its time course, and to examine the role of humoral factor in the SAD induced aortic remodeling. Methods: In rats with chronic SAD or sham operation, aortic structure was measured by computer image analysis, aortic function by isolated artery preparation, and angiotensinⅡ concentration by radioimmunoassay. Results and Conclusion: (1)The aortic structural remodeling developed progressively 4, 8, 16 and 32 weeks after SAD. Aortic structural remodeling after SAD expressed was mainly aortic hypertrophy due to SMC growth and collagen accumulation. (2)The aortic contraction elicited by norepinephrine (NE) was progressively increased at 8, 16 and 32 weeks after SAD. The aortic relaxation elicited by acetylcholine (ACh) was depressed at 8, 16 and 32 weeks after SAD. In addition, we found that in 32 week SAD rats the NE induced contraction was not increased by endothelial denudation. These indicated that the increased contraction and depressed relaxation after SAD were related to the change of endothelium and/or the change of interaction between endothelium and SMC. (3)In 10 week SAD rats, plasma angiotensinⅡ concentration remained unchanged, whereas aortic angiotensinⅡ concentration was significantly increased, suggesting that activation of tissue renin angiotensin system may be involved in SAD induced aortic remodeling. [
关 键 词:去窦弓神经 主动脉重建 肾素-血管紧张素系统
分 类 号:R543.1[医药卫生—心血管疾病]
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