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Updated: May 24, 2025
Location, Dissection, and Analysis of the Murine Stellate Ganglion
Published on: December 22, 2020
Stellate Ganglionectomy Attenuates Pressure Overload-Induced Cardiac Hypertrophy and Dysfunction
Hui Yan1, Xiujun Li2, Beilei Liu2
1Department of Pharmacy, Wuhan No.1 Hospital, 430022 Wuhan, Hubei, China.
Insights
Stellate ganglionectomy significantly improved cardiac function and reduced hypertrophy in a pressure overload rat model. This procedure likely inhibits the CaMKII/RyR2 pathway, offering a potential therapy for heart failure.
Area of Science:
- Cardiovascular Research
- Neuroscience
- Physiology
Background:
- Enhanced cardiac sympathetic activity is a key factor in chronic heart failure (CHF).
- Stellate ganglion (SG) interventions can modulate sympathetic activity, potentially impacting cardiovascular disease progression.
- This study investigates stellate ganglionectomy's effects on pressure overload-induced myocardial hypertrophy and dysfunction.
Purpose of the Study:
- To evaluate the therapeutic potential of stellate ganglionectomy in mitigating pressure overload-induced cardiac damage.
- To elucidate the underlying molecular mechanisms, including the CaMKII/RyR2 pathway, affected by stellate ganglionectomy.
Main Methods:
- A rat model of pressure overload was established using abdominal aortic constriction.
- Four experimental groups were utilized: sham surgery, aortic constriction (AB), left stellate ganglionectomy (LSG), and right stellate ganglionectomy (RSG).
- Cardiac function, myocardial hypertrophy, fibrosis, neurohormonal markers (ANP, NE), and key molecular signaling pathways (CaMKII/RyR2) were assessed.
Main Results:
- Stellate ganglionectomy significantly improved cardiac function, evidenced by increased ejection fraction (LVEF) and fractional shortening (LVFS), and reduced ventricular dimensions.
- Histological analysis revealed decreased myocardial hypertrophy and fibrosis in the SG-ablated groups.
- Molecular analyses demonstrated reduced norepinephrine levels and inhibition of the CaMKII/RyR2 signaling pathway.
Conclusions:
- Stellate ganglionectomy effectively alleviates cardiac hypertrophy and dysfunction in a pressure overload model.
- The observed benefits are likely mediated by the inhibition of the CaMKII/RyR2 pathway and reduced sympathetic drive.
- Stellate ganglionectomy presents a promising therapeutic strategy for managing heart failure associated with increased sympathetic activity.
Background:
Enhanced cardiac sympathetic activity contributes to chronic heart failure (CHF). Interventions targeting the stellate ganglion (SG) can reduce this activity, potentially slowing the progression of cardiovascular diseases. This study examined the effects and mechanisms of stellate ganglionectomy on myocardial hypertrophy and cardiac dysfunction caused by pressure overload.
Methods:
A rat model of pressure overload was created using abdominal aortic constriction. Four groups were studied: the sham surgery, abdominal aortic coarctation (AB), aortic constriction plus left stellate ganglionectomy (LSG), and aortic constriction plus right stellate ganglionectomy (RSG) groups. Cardiac function was assessed via echocardiography, and myocardial hypertrophy and fibrosis were evaluated using hematoxylin-eosin staining (H&E) and Masson staining. Serum atrial natriuretic peptides (ANP) and norepinephrine (NE) levels were measured using enzyme linked immunosorbent assay (ELISA), and the levels of the molecular markers tyrosine hydroxylase (TH) and growth-associated protein-43 (GAP43) were analyzed using Western blotting and PCR. Calcium calmodulin dependent protein kinase II (CaMKII) and phosphorylated Ryanodine Receptor 2 (p-RyR2) expression were also investigated.
Results:
Stellate ganglionectomy significantly reduced myocardial hypertrophy and improved cardiac function, as indicated by decreased left ventricular posterior wall thickness (LVPWD) (p < 0.01), left ventricular end-diastolic diameter (LVEDD) and volume (p < 0.001), left ventricular end-diastolic volume (LVEDV) (p < 0.001), increased left ventricular ejection fraction (LVEF) (p < 0.001) and left ventricular fractional shortening (LVFS) (p < 0.001). Histological analysis confirmed reduced myocardial dilation. Molecular analysis revealed decreased CaMKII/RyR2 signaling (p < 0.001) and lower NE levels (p < 0.01), suggesting reduced neurohormonal stress.
Conclusions:
Stellate ganglionectomy alleviates hypertrophy and cardiac dysfunction caused by pressure overload, likely through inhibition of the CaMKII/RyR2 pathway, underscoring its potential as a therapeutic approach.
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