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Published on: April 13, 2018
Chronic Stress Facilitates the Development of Deep Venous Thrombosis
Tao Dong1, Yu-Wen Cheng1, Fei Yang2
1Department of Physiology, Medical College of Soochow University, Suzhou 215003, China.
Insights
Chronic stress promotes deep venous thrombosis (DVT) via renal sympathetic nerves and oxidative stress. Treatments like renal sympathetic denervation or antioxidants can alleviate DVT development and platelet activation.
Area of Science:
- Cardiovascular Science
- Neuroscience
- Physiology
Background:
- Modern social stress exacerbates cardiovascular diseases, including deep venous thrombosis (DVT).
- Renal sympathetic denervation is a treatment for resistant hypertension.
- Oxidative stress is closely linked to cardiovascular disease development.
Purpose of the Study:
- To investigate the mechanisms linking the renal sympathetic nerve system and oxidative stress to blood coagulation in DVT.
- To explore the role of these factors in DVT development under chronic stress conditions.
Main Methods:
- A chronic foot shock model in rats was used to simulate physiological stress.
- Deep venous thrombosis (DVT) and platelet aggregation were assessed.
- Effects of renal sympathetic denervation and antioxidant (Tempol) treatment were evaluated.
- Circulating oxidation factors were measured.
Main Results:
- Chronic foot shock promoted DVT, likely through platelet aggregation.
- Renal sympathetic denervation and Tempol treatment alleviated DVT aggravation and platelet activation.
- Denervation reduced circulating oxidation factors.
Conclusions:
- Both renal sympathetic nerve activity and oxidative stress contribute to DVT development under chronic stress.
- These findings suggest potential novel therapeutic strategies for clinical DVT patients.
Abstract:
The increasing pressure of modern social life intensifies the impact of stress on the development of cardiovascular diseases, which include deep venous thrombosis (DVT). Renal sympathetic denervation has been applied as one of the clinical approaches for the treatment of drug-resistant hypertension. In addition, the close relationship between oxidative stress and cardiovascular diseases has been well documented. The present study is designed to explore the mechanism by which the renal sympathetic nerve system and the oxidative stress affect the blood coagulation system in the development of DVT. Chronic foot shock model in rats was applied to mimic a state of physiological stress similar to humans. Our results showed that chronic foot shock procedure could promote DVT which may be through the activation of platelets aggregation. The aggravation of DVT and activation of platelets were alleviated by renal sympathetic denervation or antioxidant (Tempol) treatment. Concurrently, the denervation treatment could also reduce the levels of circulating oxidation factors in rats. These results demonstrate that both the renal sympathetic nerve system and the oxidative stress contribute to the development of DVT in response to chronic stress, which may provide novel strategy for treatment of clinic DVT patients.
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