Figure legends:
Figure 1: Flow chart of the study protocol
HF=Heart failure; LL-ES=Low-level electrical stimulation; ARVGP=aortic
root ventricular ganglionated plexi; TG-β=transforming growth
factor-beta; MMP-9=matrix metalloproteinase-9; AT-1R=angiotensin II type
I receptor; p-ERK1/2=phosphorylated extracellular signal-regulated
kinase; VERP=ventricular effective refractory period; LVEDV=left
ventricular end-diastolic volume; LVESV=left ventricular end-systolic
volume; LVSV=left ventricular stroke volume; LVEF=left ventricular
ejection fraction.
Figure 2: Comparison of arrhythmic incidences before and after LL-ES
ARVGP
At baseline HF status, the inducing rate of arrhythmia presented almost
no difference among the control, drug, and LL-ES groups. However, after
1 week of treatment, the inducing rate of arrhythmia remained at 80% in
the control group but dropped to 60 % in the drug group and to 10 % in
the LL-ES group.
Abbreviations see figure 1.
Figure 3: Change of protein levels in HF factors after LL-ES ARVGP
A: Compared with the control group, TGF-β, MMP-9, and AT-1R protein
levels decreased significantly while the expression of p-ERK1/2 was not
significantly different after 1 week of drug administration. However,
compared with the drug group, TGF-β, MMP-9, and AT-1R protein levels
reduced significantly, and the expression of p-ERK1/2 increased
remarkably after 1 week of LL-ES ARVGP.
Abbreviations see figure 1.
Figure 4: Effect of LL-ES of ARVGP on protein expression in the LV
Compared with drug group, TGF-β, MMP-9, and AT-1R protein expression
levelsdown-regulated significantly whilethe level of p-ERK1/2 increased
remarkedly after 1 week of LL-ES ARVGP. GAPDH was used as a loading
control.
Abbreviations see figure 1.