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Published on: June 29, 2014
Early structural changes of aortic wall in sinoaortic-denervated rats
Fu-Ming Shen1, Shu-Hui Zhang, He-Hui Xie
1Department of Pharmacology, Second Military Medical University, Shanghai, China.
Clinical and Experimental Pharmacology & Physiology
|April 20, 2006
Summary
Sinoaortic denervation (SAD) in rats significantly increases blood pressure variability and causes early structural damage to the aortic wall, including endothelial cell apoptosis and reduced eNOS expression. These changes may prime the aorta for further organ damage.
Area of Science:
- Cardiovascular Physiology
- Vascular Biology
- Surgical Research
Background:
- Sinoaortic denervation (SAD) is a surgical procedure that affects autonomic regulation of blood pressure.
- Understanding the early structural aortic wall changes post-SAD is crucial for comprehending subsequent organ damage.
Purpose of the Study:
- To investigate the time-course of early structural alterations in the aortic wall following sinoaortic denervation (SAD) in Sprague-Dawley rats.
- To correlate observed aortic changes with alterations in blood pressure variability (BPV).
Main Methods:
- Rats underwent SAD or sham operation, with examinations at 1, 2, and 4 weeks post-procedure.
- Assessments included blood pressure monitoring, light and electron microscopy, immunohistochemistry, and TUNEL assay.
- Quantification of smooth muscle cell density (SMC%), collagen density (CD%), and aortic wall thickness (WT) were performed.
Main Results:
- SAD significantly increased blood pressure variability (BPV) at all time points compared to sham controls.
- Aortic smooth muscle cell density (SMC%) increased by 2 weeks post-SAD.
- By 4 weeks, SAD induced increased SMC%, collagen density (CD%), aortic wall thickness (WT), endothelial cell degeneration, apoptosis, and reduced eNOS expression.
Conclusions:
- This study provides the first detailed timeline of aortic wall and endothelial cell changes after SAD.
- Elevated BPV following SAD appears to be a critical initiating factor for aortic structural damage and potential organ injury.
