Neurogastroenterology and motility · 2018
Electroacupuncture via chronically implanted electrodes improves gastric dysmotility mediated by autonomic-cholinergic mechanisms in a rodent model of functional dyspepsia.
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Zhang S, Li S, Liu Y, Ye F, Yin J, Foreman R D, Wang D, Chen J D Z
Аннотация
BACKGROUND: Electroacupuncture (EA) has been shown to be effective in reducing symptoms in patients with functional dyspepsia (FD). However, its mechanisms remain largely unknown. The aim of this study was to investigate mechanisms of the prokinetic effects of EA in a rodent model of FD.
METHODS: A FD model was established by neonatal treatment of iodoacetamide (IA). Eight weeks later, the rats were implanted with electrodes in the stomach for the measurement of gastric slow waves (GSW) and electrodes into acupoints ST36 for EA. Autonomic functions were assessed by the spectral analysis of heart rate variability.
KEY RESULTS: (i) The IA-treated rats ("FD" rats) showed increased dysrhythmia in both fasting and fed states (P < .01) as well as during rectal distention (P < .02). EA reduced the percentage of dysrhythmia (P < .05 for both fasting and fed) and normalized RD-induced impairment in GSW in "FD" rats. Atropine blocked the effect of EA on GSW. (ii) "FD" rats showed delayed gastric emptying (P = .001 vs control) that was accelerated with EA (P = .01, vs sham-EA). (iii) "FD" rats showed increased plasma norepinephrine (P = .006, vs control) that was suppressed with EA (P = .003) and reduced vagal activity that was improved with EA.
CONCLUSIONS AND INFERENCES: Gastric motility (GSW and GE) is impaired in rats treated with IA, possibly attributed to impaired autonomic functions. EA improves GSW and accelerates GE mediated via the autonomic and cholinergic mechanisms.
METHODS: A FD model was established by neonatal treatment of iodoacetamide (IA). Eight weeks later, the rats were implanted with electrodes in the stomach for the measurement of gastric slow waves (GSW) and electrodes into acupoints ST36 for EA. Autonomic functions were assessed by the spectral analysis of heart rate variability.
KEY RESULTS: (i) The IA-treated rats ("FD" rats) showed increased dysrhythmia in both fasting and fed states (P < .01) as well as during rectal distention (P < .02). EA reduced the percentage of dysrhythmia (P < .05 for both fasting and fed) and normalized RD-induced impairment in GSW in "FD" rats. Atropine blocked the effect of EA on GSW. (ii) "FD" rats showed delayed gastric emptying (P = .001 vs control) that was accelerated with EA (P = .01, vs sham-EA). (iii) "FD" rats showed increased plasma norepinephrine (P = .006, vs control) that was suppressed with EA (P = .003) and reduced vagal activity that was improved with EA.
CONCLUSIONS AND INFERENCES: Gastric motility (GSW and GE) is impaired in rats treated with IA, possibly attributed to impaired autonomic functions. EA improves GSW and accelerates GE mediated via the autonomic and cholinergic mechanisms.