Implanted Electrodes on St 36 improve gastic mobility and HRV
Kristen Sparrow • November 09, 2019
Acupuncture improves gastric motility and HRV in an animal model of chemically induces gastroparesis
This study looked at an animal model of functional dysmotility caused in utero and then after 2 months of life implant electrodes at St 36. The electrodes not only cause improved motility, but lower norepinephrine and improved HRV also.
We may see a time soon when implanted electrodes and remote stimulation aid in reinforcing acupuncture treatment
Electroacupuncture via chronically implanted electrodes improves gastric dysmotility mediated by autonomic-cholinergic mechanisms in a rodent model of functional dyspepsia.
Author information
- 1
- Veterans Research and Education Foundation, VA Medical Center, Oklahoma City, OK, USA.
- 2
- Department of Physiology, University of Oklahoma Health Science Center, Oklahoma City, OK, USA.
- 3
- Department of Gastroenterology, Tianjin No. 254 Hospital, Tianjin, China.
- 4
- Division of Gastroenterology and Hepatology, Johns Hopkins Center for Neurogastroenterology, Baltimore, MD, USA.
- 5
- Department of traditional Chinese medicine, 1st Affiliated Hospital of Xi’an Jiao tong University, Xi’an, Shannxi, China.
- 6
- Department of Hepatology, 1st Affiliated Hospital of Xi’an Jiao Tong University, Xi’an, Shannxi, China.
Abstract
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.
