• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

去窦弓神经大鼠主动脉壁的早期结构变化。

Early structural changes of aortic wall in sinoaortic-denervated rats.

作者信息

Shen Fu-Ming, Zhang Shu-Hui, Xie He-Hui, Jing Qing, Wang Di-Song, Su Ding-Feng

机构信息

Department of Pharmacology, Second Military Medical University, Shanghai, China.

出版信息

Clin Exp Pharmacol Physiol. 2006 Apr;33(4):358-63. doi: 10.1111/j.1440-1681.2006.04375.x.

DOI:10.1111/j.1440-1681.2006.04375.x
PMID:16620301
Abstract
  1. The present work was designed to observe the early structural changes in the aortic wall in Sprague-Dawley rats 1, 2 and 4 weeks after sinoaortic denervation (SAD). 2. Rats were examined 1, 2 and 4 weeks after SAD. Blood pressure (BP) was recorded in the conscious state. The thoracic aortas were taken for investigations, including: light microscopy, electron microscopy, immunohistochemistry and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labelling (TUNEL). 3. Blood pressure variability (BPV) was significantly increased in the SAD groups 1, 2 and 4 after the operation when compared with the sham-operated ones. 4. Two weeks after SAD the percentage proportion of smooth muscle cell density (SMC%) was obviously increased. 5. Four weeks after SAD: the SMC%, percentage proportion of collagen density (CD%) and aortic wall thickness (WT) were obviously increased with vascular smooth muscle cells blebbing concomitantly. Endothelial cells showed degenerative changes and swelling with blebbing of the cell membrane and increased condensation of peripheral nuclear chromatin and cytoplasmic vacuolization. It was also found that the number of apoptotic endothelial cells was increased and expression of eNOS was reduced. 6. This is the first study that shows the time-course of aortic wall and endothelial cell changes induced by SAD. Increased BPV might be the priming factor in the development of organ damage induced by SAD.
摘要
  1. 本研究旨在观察去窦弓神经支配(SAD)后1周、2周和4周的Sprague-Dawley大鼠主动脉壁的早期结构变化。2. 在SAD后1周、2周和4周对大鼠进行检查。在清醒状态下记录血压(BP)。取出胸主动脉进行研究,包括:光学显微镜检查、电子显微镜检查、免疫组织化学和末端脱氧核苷酸转移酶(TdT)介导的dUTP缺口末端标记(TUNEL)。3. 与假手术组相比,SAD组术后1周、2周和4周的血压变异性(BPV)显著增加。4. SAD后两周,平滑肌细胞密度百分比(SMC%)明显增加。5. SAD后四周:SMC%、胶原密度百分比(CD%)和主动脉壁厚度(WT)明显增加,同时血管平滑肌细胞出现气泡样改变。内皮细胞出现退行性变化和肿胀,细胞膜出现气泡样改变,外周核染色质凝聚增加,细胞质空泡化。还发现凋亡内皮细胞数量增加,内皮型一氧化氮合酶(eNOS)表达降低。6. 这是第一项显示SAD诱导的主动脉壁和内皮细胞变化时间进程的研究。血压变异性增加可能是SAD诱导器官损伤发展的启动因素。

相似文献

1
Early structural changes of aortic wall in sinoaortic-denervated rats.去窦弓神经大鼠主动脉壁的早期结构变化。
Clin Exp Pharmacol Physiol. 2006 Apr;33(4):358-63. doi: 10.1111/j.1440-1681.2006.04375.x.
2
Down-regulation of DDAH2 and eNOS induces endothelial dysfunction in sinoaortic-denervated rats.下调 DDAH2 和 eNOS 可导致去窦弓神经大鼠的血管内皮功能障碍。
Eur J Pharmacol. 2011 Jul 1;661(1-3):86-91. doi: 10.1016/j.ejphar.2011.04.041. Epub 2011 Apr 28.
3
Fosinopril prevents the pulmonary arterial remodeling in sinoaortic-denervated rats by regulating phosphodiesterase.福辛普利通过调节磷酸二酯酶预防去窦弓神经大鼠的肺动脉重塑。
J Cardiovasc Pharmacol. 2008 Jan;51(1):24-31. doi: 10.1097/FJC.0b013e318159e097.
4
Circadian expression of clock genes and angiotensin II type 1 receptors in suprachiasmatic nuclei of sinoaortic-denervated rats.去窦弓神经大鼠视交叉上核中时钟基因和血管紧张素II 1型受体的昼夜节律性表达
Acta Pharmacol Sin. 2007 Apr;28(4):484-92. doi: 10.1111/j.1745-7254.2007.00543.x.
5
Blood pressure variability increases connexin expression in the vascular smooth muscle of rats.血压变异性增加大鼠血管平滑肌中连接蛋白的表达。
Cardiovasc Res. 2008 Oct 1;80(1):123-30. doi: 10.1093/cvr/cvn178. Epub 2008 Jul 1.
6
Activation of receptor for advanced glycation end products contributes to aortic remodeling and endothelial dysfunction in sinoaortic denervated rats.晚期糖基化终产物受体的激活导致去窦弓神经大鼠主动脉重构和内皮功能障碍。
Atherosclerosis. 2013 Aug;229(2):287-94. doi: 10.1016/j.atherosclerosis.2013.04.033. Epub 2013 May 9.
7
Greater hypertrophy in right than left ventricles is associated with pulmonary vasculopathy in sinoaortic-denervated Wistar-Kyoto rats.在去窦主动脉神经支配的Wistar-Kyoto大鼠中,右心室比左心室更大的肥厚与肺血管病变相关。
Clin Exp Pharmacol Physiol. 2004 Jul;31(7):450-5. doi: 10.1111/j.1440-1681.2004.04023.x.
8
Protection of organic trauma in sinoaortic-denervated rats treated with fosinopril.福辛普利治疗去窦弓神经大鼠有机损伤的保护作用
Yao Xue Xue Bao. 2003 Oct;38(10):743-7.
9
[Autoregulation of renal blood flow and blood pressure variability in the conscious rat].[清醒大鼠肾血流量的自身调节与血压变异性]
Arch Mal Coeur Vaiss. 2001 Aug;94(8):818-21.
10
Apoptosis is involved in the cardiac damage induced by sinoaortic denervation in rats.
Clin Exp Pharmacol Physiol. 2003 May-Jun;30(5-6):362-8. doi: 10.1046/j.1440-1681.2003.03840.x.

引用本文的文献

1
Arterial baroreflex dysfunction impairs ischemia-induced angiogenesis.动脉压力反射功能障碍会损害缺血诱导的血管生成。
J Am Heart Assoc. 2014 May 12;3(3):e000804. doi: 10.1161/JAHA.114.000804.
2
Role of Kir6.2 subunits of ATP-sensitive potassium channels in endotoxemia-induced cardiac dysfunction.ATP 敏感性钾通道 Kir6.2 亚基在内毒素血症诱导的心脏功能障碍中的作用。
Cardiovasc Diabetol. 2013 May 9;12:75. doi: 10.1186/1475-2840-12-75.
3
Contribution of hydrogen sulfide and nitric oxide to exercise-induced attenuation of aortic remodeling and improvement of endothelial function in spontaneously hypertensive rats.
硫化氢和一氧化氮对运动诱导的自发性高血压大鼠主动脉重构的抑制作用及其对内皮功能的改善作用。
Mol Cell Biochem. 2013 Mar;375(1-2):199-206. doi: 10.1007/s11010-012-1542-1. Epub 2012 Dec 15.
4
Mimecan is involved in aortic hypertrophy induced by sinoaortic denervation in rats.Mimecan 参与了大鼠主动脉神经切断诱导的主动脉肥大。
Mol Cell Biochem. 2011 Jun;352(1-2):309-16. doi: 10.1007/s11010-011-0767-8. Epub 2011 Apr 26.
5
The combination of atenolol and amlodipine is better than their monotherapy for preventing end-organ damage in different types of hypertension in rats.在预防大鼠不同类型高血压的终末器官损伤方面,阿替洛尔和氨氯地平联合用药比单一用药效果更好。
J Cell Mol Med. 2009 Apr;13(4):726-34. doi: 10.1111/j.1582-4934.2008.00365.x. Epub 2009 Feb 12.