Superior cervical gangliectomy exacerbates the aortic dissection in mice.

Abstract

Sympathetic innervation is fundamentally required for physiological aortic homeostasis. Though it plays a vital important role in aortic function, its specific role in aortic dissection (AD) remains unclear. In this study, we explored the role of the sympathetic nervous system in AD by examining the effects of superior cervical ganglionectomy (SCGx) in mice. Using β-aminopropionitrile (BAPN) induced AD mice model at pre-lesional stage, the tyrosine hydroxylase (TH) expression, indicative of sympathetic activity, increased early in AD progression and correlated with aortic elastic lamina degradation. SCGx did not affect aortic structure within 2 weeks without BAPN treatment, but bilateral SCGx exacerbated AD severity, increasing rupture rates and tear range after BAPN and angiotensin II (AngII) treatment. These findings highlighted the role of sympathetic nervous system in early AD stages and suggested bilateral SCGx may negatively impact AD progression. Furthermore, we found a trend toward smooth muscle cell phenotypic transformation after implementing SCGx in AD, revealing the integrity of the SCG played a pivotal role in preserving aortic homeostasis.