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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.

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。

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