Bilateral sympathetic stellate ganglionectomy attenuates myocardial remodelling and fibrosis in a rat model of chronic volume overload

Figures

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  Figure 1. A, The stellate ganglion was exposed under the surgical microscope. All nerve branches running into the ganglion and the ganglion were isolated and excised (a, ×10). The ganglion was processed for paraffin embedding and sliced into 4 μm tissue sections, stained blue with Nissl staining (Arrow) (b, ×200). B, Protein expression of sympathetic neurohormones in RV. Protein expression of TH, NPY, GAP43 and PGP9.5 in RV were up‐regulated in AV group (vs S group) and protein expression of GAP43 and PGP9.5 was down‐regulated in AD group (vs AV group) (*P < 0.05,**P < 0.01). (S, AV and AD, n = 4). C, Immunohistochemistry staining of sympathetic neurohormones in RV. The protein expression of TH, NPY, GAP43 (**P < 0.01) and PGP9.5 (*P < 0.05) was increased in AV group (vs S group) and protein expression of GAP43 (**P < 0.01) was reduced in AD group compared to AV group in RV (×400). (S, AV and AD, n = 3)

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  Figure 2. A, Protein expression of sympathetic neurohormones in LV. Protein expression of GAP43 and PGP9.5 tended to be higher in AV group compared to S group in LV (P = 0.067, P = 0.088). (S, AV and AD, n = 4). B, Immunohistochemistry staining of sympathetic neurohormones in LV. The protein expression of NPY (**P < 0.01), TH, GAP43 and PGP9.5 (*P < 0.05) were significantly increased in AV group compared to S group in LV (×400). (S, AV and AD, n = 3)

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  Figure 3. A, Echocardiography results. (a) LVIDd, LV internal diameter at end‐diastole; (b) LVIDs, LV internal diameter at end‐systole; (c) EF, ejection fraction; (d) FS, fractional shortening (**P < 0.01). (S, n = 7; AV, n = 7; AD, n = 8). B, Gross heart morphology. Ventricular enlargement and cardiac hypertrophy in the AV and AD group. (S, AV and AD, n = 3)

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  Figure 4. A, Cardiomyocyte size measured on HE stained sections. The cardiomyocyte cross‐sectional area of RV and LV enlarged in AV group compared to S group and was significantly smaller in RV of AD group (*P < 0.05, ×400). (S, AV and AD, n = 3). B, mRNA expressions of myocardial ANP and BNP in right and left ventricle. mRNA expression of ANP and BNP in RV was significantly up‐regulated in AV group compared to S group, ANP expression was significantly down‐regulated in AD group compared to AV group in RV (a and b, **P < 0.01), mRNA expression of ANP and BNP in LV was similar among groups (c and d). Quantification graph are shown from triplicate experiments. (S, AV and AD, n = 4)

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  Figure 5. A, Percentage of collagen deposited in myocardial extracellular matrix. Percentage of collagen deposited in myocardial extracellular matrix in RV and LV determined on Sirius red stained sections (×400) (*P < 0.05,**P < 0.01). (S, AV and AD, n = 3). B, Myocardial fibrosis cytokines expression in RV. mRNA expression of ɑ‐SMA, fibronectin, collagen I and III was increased in RV of AV group and mRNA expression of collagen I was down‐regulated in AD group (a,b,c and d, *P < 0.05). Protein expression of collagen I was up‐regulated in AV group and down‐regulated in AD group in RV (e, *P < 0.05, **P < 0.01), while protein expression of collagen III in RV was similar among groups (f). Quantification graph are shown from triplicate experiments. (S, AV and AD, n = 4). C, Myocardial fibrosis cytokines expression in LV. mRNA expression of collagen III was increased in LV of AV group (d, *P < 0.05). Myocardial fibrosis protein expression in LV was similar in various groups in LV (e and f). Quantification graph are shown from triplicate experiments. (S, AV and AD, n = 4)

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  Figure 6. Immunohistochemistry staining of Ang II and aldosterone in RV and LV. Protein expression of Ang II and aldosterone was increased in AV group in RV and LV, and down‐regulated in AD group in RV (*P < 0.05, **P < 0.01, ×400). Protein expression of Ang II was also down‐regulated in AD group in LV. (S, AV and AD, n = 3)