Cardiac sympathetic afferent denervation improves cardiac post-ischemic remodeling by maintaining autonomic tone

Figures

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  Fig. 1. Neural recording from LSG activity. (A) Representative examples of LSG neural activity from the three groups. (B) The average frequency of LSG activity were significantly increased in MI group, while treatment with CSAD obviously mitigated the increase of LSG activity induced by MI. (C) The average amplitude of LSG activity were significantly increased in MI group, while treatment with CSAD obviously mitigated the increase of LSG activity induced by MI. CSAD, cardiac sympathetic afferent denervation; LSG, left stellate ganglion; MI, myocardial infarction. n = 9 animals for all comparisons.

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  Fig. 2. HRV analysis from the three groups at baseline and 4 weeks Compared to the Control group, the MI group demonstrated a significant increase in LF power (A) and LF/HF ratio (C), accompanied by a slight reduction in HF power (B). In contrast, treatment with CSAD significantly attenuated the upward trends observed in the LF/HF ratio, while simultaneously increasing HF power. CSAD, cardiac sympathetic afferent denervation; HF, high frequency; HRV, heart rate variability; LF, low frequency. n = 9 animals for all comparisons.

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  Fig. 3. Immunohistochemistry analysis of LSG tissues at 4 weeks. A: Representative examples of TH in the LSG from the three groups. B: treatment with CSAD substantially increased the average percentage of TH-negative ganglionic cells in the LSG compared to the MI group. C: administration of CSAD significantly decreased the expression of TH-positive ganglionic cells in the LSG when compared to the MI group. These TH-negative neurons are indicated by yellow arrows. CSAD, cardiac sympathetic afferent denervation; LSG, left stellate ganglion; MI, myocardial infarction; TH, tyrosine hydroxylase. n = 9 animals for all comparisons. Yellow arrows indicated TH-negative ganglionic cells (lacking brown cytoplasmic staining), while brown cells with distinct cytoplasmic staining were identified as TH-positive.

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  Fig. 4. Impact of CSAD on the plasma levels of hs-CRP, NE, NT-proBNP, and NPY. The induction of MI resulted in a significant increase in plasma levels of hs-CRP (A), NE (B), NT-proBNP (C), and NPY (D) (all p < 0.05). However, treatment with CSAD effectively mitigated the elevation of hs-CRP, NE, NT-proBNP, and NPY levels induced by MI (all p < 0.05). CSAD, cardiac sympathetic afferent denervation; hs-CRP, high-sensitivity C-reactive protein; NE, Norepinephrine; NPY, neuropeptide Y; NT-proBNP, N-terminal pro-B-type natriuretic peptide; n = 9 animals for all comparisons.

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  Fig. 5. The transthoracic echocardiographic evaluation conducted at baseline and 4 weeks. The MI group exhibited a significant increase in left ventricular EDV and ESV, along with a significant decrease in LVEF and E/A ratio. The treatment with CSAD significantly reduced the dilation of EDV and ESV, and increased LVEF and E/A ratio compared to the MI group. CSAD, cardiac sympathetic afferent denervation; E/A: Peak mitral inflow velocity in early diastole (E) / peak mitral inflow velocity during left atrial contraction (A); EDV: Left ventricular end-diastolic volume; ESV: Left ventricular end-systolic volume; LVEF: left ventricular ejection fraction; MI, myocardial infarction.

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  Fig. 6. Impact of CSAD treatment on proteins expression. A: Representative image of western blots conducted on non-infarcted tissues of the LV from the three groups. The protein analyses provide insights into the relative levels of TGF-β1 (B), MMP-9 (C), Collagen-I (D), and Collagen-III (E). The MI group exhibited increased protein levels of TGF-β1, MMP-9, Collagen-I, and Collagen-III compared to the Control group (all p < 0.05). However, the administration of CSAD significantly attenuated the elevated protein levels of TGF-β1, MMP-9, Collagen-I, and Collagen-III in comparison to the MI group (all p < 0.05). CSAD, cardiac sympathetic afferent denervation; MI, myocardial infarction; MMP-9, matrix metallopeptidase 9; TGF-β1, transforming growth factor-beta. n = 3 animals for comparisons.